DOING AC

TAKING RECOVERY TO THE STREETS

On the Sunday before Christmas, members of the recovery community will host a holiday event with specific healing goals in mind. 

1. To begin to lower the risk of Atlantic City's kids for developing a substance use disorder.

2.  To recognize the recovery support needs of parents and other family members during the holidays who have lost someone they love to the epidemic.

3.  To provide a full holiday event experience for families new in recovery to help avoid the holiday stressors of commercialism. 

4.  To embrace those still struggling by bringing recovery to their streets.

On Sunday, December 22, 2019 HOPE for the Holidays - Atlantic City will take place from 10am - 6pm on South Tennessee Avenue as a new holiday tradition featuring the TREE OF HOPE.  

 


INTERESTED IN HELPING ATLANTIC CITY RISE UP?

IN THE NEWS.....

At 32, Raquel Bennett was looking for a reason to live. She’d struggled with severe depression for more than a decade, trying multiple antidepressants and years of talk therapy. The treatment helped, but not enough to make it seem worth living with a debilitating mental illness, she says. “I was desperate.”In 2002, following a friend’s suggestion, Bennett received an injection of ketamine, an anesthetic and psychedelic party drug also known as Special K. During her first ketamine trip, Bennett hallucinated that God inserted a giant golden key into her ear, turning on her brain. “It was as if I was living in a dark house and suddenly the lights came on,” she says. “Suddenly everything seemed illuminated.”The drug lifted Bennett’s depression and dispelled her thoughts of suicide within minutes. The effect lasted for several months, and, she says, the respite saved her life. She was fascinated by the drug’s rapid effects and went on to earn a doctoral degree in psychology, writing her dissertation about ketamine. Today, she works at a clinic in Berkeley, California, that specializes in using ketamine to treat depression. “This medicine works differently and better than any other medication I’ve tried,” she says.When Bennett experimented with ketamine, the notion of using a psychedelic rave drug for depression was still decidedly fringe. Since the first clinical trials in the early 2000s, however, dozens of studies have shown that a low dose of ketamine delivered via IV can relieve the symptoms of depression, including thoughts of suicide, within hours.Even a low dose can have intense side effects, such as the sensation of being outside one’s body, vivid hallucinations, confusion and nausea. The antidepressant effects of ketamine typically don’t last more than a week or two. But the drug appears to work where no others have — in the roughly 30 percent of people with major depression who, like Bennett, don’t respond to other treatments. It also works fast, a major advantage for suicidal patients who can’t wait weeks for traditional antidepressants to kick in.“When you prescribe Prozac, you have to convince people that it’s worth taking a medication for several weeks,” says John Krystal, a psychiatrist and neuroscientist at Yale University in New Haven, Connecticut. “With ketamine, patients may feel better that day, or by the next morning.”The buzz around ketamine can drown out just how little is known about the drug. In the April 2017 JAMA Psychiatry, the American Psychiatric Association published an analysis of the evidence for ketamine treatment noting that there are few published data on the safety of repeated use, although studies of ketamine abusers — who typically use much higher doses — show that the drug can cause memory loss and bladder damage. Most clinical trials of the low dose used for depression have looked at only a single dose, following up on patients for just a week or two, so scientists don’t know if it’s safe to take the drug repeatedly over long periods. But that’s exactly what might be necessary to keep depression at bay.The analysis also warned about ketamine’s well-established potential for abuse. Used recreationally, large doses of the drug are known to be addictive — there’s some evidence that ketamine can bind to opioid receptors, raising alarms that even low doses could lead to dependence.Bennett has now been receiving regular ketamine injections for 17 years, with few negative side effects, she says. She doesn’t consider herself addicted to ketamine because she feels no desire to take it between scheduled appointments. But she does feel dependent on the drug, in the same way that a person with high blood pressure takes medication for hypertension, she says.Still, she acknowledges what most clinicians and researchers contend: There simply aren't enough data to know what the optimal dose for depression is, who is most likely to benefit from ketamine treatment and what long-term treatment should look like. “There’s a lot that we don’t know about how to use this tool,” Bennett says. “What’s the best dose? What’s the best route of administration? How frequently do you give ketamine treatment? What does maintenance look like? Is it OK to use this in an ongoing way?”Despite the unknowns, pharmaceutical companies have been racing to bring the first ketamine-based antidepressant to market. In March, the US Food and Drug Administration approved a ketamine-derived nasal spray, esketamine, developed by Janssen Pharmaceuticals, a subsidiary of Johnson & Johnson. Only two of Janssen’s five phase III trials had shown a benefit greater than taking a placebo. Still, in February an independent panel recommended FDA approval. That makes ketamine the first novel depression drug to hit the market in more than 50 years, notes Carlos Zarate Jr, a psychiatrist who studies mood disorder therapies at the National Institute of Mental Health.Thousands of people are already flocking to private clinics like Bennett’s, which provide intravenous ketamine infusions. Because the drug was approved in the 1970s as an anesthetic, physicians can legally provide the drug as an “off-label” depression treatment. Many ketamine clinics have long waiting lists or are so swamped that they aren’t accepting new patients, and Janssen’s nasal spray could rapidly expand access to treatment.But some researchers worry that the nasal spray won’t solve many of ketamine’s problems and could create new ones. Although the FDA is requiring that the nasal spray be administered only in a certified doctor’s office or clinic, esketamine is “every bit as habit forming as regular ketamine,” and will be difficult to keep out of the hands of abusers, says Scott Thompson, a neuroscientist at the University of Maryland and a coauthor with Zarate of a 2019 review on fast-acting antidepressants in the Annual Review of Pharmacology and Toxicology. A nasal spray can’t deliver as precise a dose as an IV infusion, Thompson notes. “If someone has got a cold, they’re not going to get the same dose.”In Thompson’s view, esketamine holds few advantages over generic ketamine, which costs less than a dollar per dose, although the IV infusions in private clinics often cost hundreds of dollars per visit. Janssen has indicated that each esketamine treatment will range from $590 to $885, not including the costs of administration and observation. Zarate and others are still thrilled to see big pharma investing in ketamine, after decades of stalled efforts to find new psychiatric drugs. “As esketamine hits the market, venture capitalists will come up with better versions and move the field forward,” Zarate says. Several drug companies are now testing other ketamine-like compounds in hopes of developing drugs that have its potent antidepressant potential without its psychedelic and dissociative side effects.Depression, fast and slowIn 2001, writer Andrew Solomon published a haunting description of the depression that derailed his early 30s: “If one imagines a soul of iron that weathers with grief and rusts with mild depression, then major depression is the startling collapse of a whole structure,” he wrote.When Solomon first fell ill, in the 1990s, many clinicians and researchers presumed that the pathological brain changes underlying depression were inherently slow to repair. This mind-set was rooted in the modest but controversial success of a class of slow-acting drugs that includes Prozac.Developed in the 1950s, the drugs were first inspired by the chance observation that a hypertension drug called reserpine – an extract of the plant Rauwolfia serpentina, or devil pepper — made people intensely depressed. After discovering that reserpine depletes monoamine neurotransmitters in the brain, including serotonin and norepinephrine, scientists hypothesized that low neurotransmitter levels cause depression. They went on to develop monoaminergic antidepressants, drugs designed to increase circulating levels of these chemicals in the brain.Today, monoaminergic antidepressants include selective serotonin reuptake inhibitors (SSRIs) such as Prozac, Lexapro and Zoloft, as well as the older and less commonly prescribed monoamine oxidase inhibitors (MAOIs) and tricyclic and tetracyclic antidepressants. Scientists have long debated whether the drugs work at all, but the most comprehensive study to date — published in The Lancet in 2018 — suggests that they do lower depression symptoms in about 60 percent of depressed people, albeit only modestly more than taking a placebo.The benefits start to show up only after several weeks of treatment, however, and roughly a third of people with major depression disorder – called treatment-resistant patients — don’t respond to at least two types of monoaminergic antidepressant.By the early 2000s, the monoamine hypothesis had unraveled. This was partly due to the antidepressants’ mediocre performance in patients, and partly to experiments which showed that depleting neurotransmitter levels in healthy people does not make people depressed. Scientists now believe that drugs like Prozac do not directly treat depression’s root cause. Instead, they think the drugs work via an indirect mechanism to subtly boost the growth of synapses and the birth of new neurons, and that this somehow relieves symptoms.Solomon’s bleak metaphor of corrosion was at least partly grounded in science. Many scientists now agree that depression slowly eats away at the neural pathways underlying our sense of worth and well-being, our desire to go to the movies or get out of bed. But research into ketamine holds out new hope that — unlike rusted iron — the depressed brain can be restored, by repairing and strengthening the neural circuits that regulate mood. —Emily UnderwoodSome researchers are also testing whether ketamine works for conditions beyond depression, such as obsessive-compulsive disorder, as well as in specific subsets of patients, such as severely depressed teenagers. Other scientists are using ketamine to help untangle one of the biggest mysteries in neuroscience: What causes depression? (See sidebar.)Seeking answers in neural wiringThirty years ago, the prevailing thought was that low levels of certain brain chemicals, such as serotonin, caused depression. Boosting those could remove symptoms.“I felt that depression needed months or weeks of treatment — that the plastic changes involved in the healing process would require weeks to reset themselves,” says Todd Gould, a neuropharmacologist at the University of Maryland and a coauthor of the recent review paper. But ketamine’s speed of action casts doubt on that idea.Newer evidence suggests that depression is caused by problems in the neural circuits that regulate mood, Gould notes. Much of the evidence for this faulty-wiring hypothesis comes from rodents. Starting in the 1990s, scientists began to discover intriguing abnormalities in the brains of mice and rats that had been exposed to certain stressors, such as bullying by a big, aggressive male.Stress and trauma are strong predictors of depression in people, but scientists can’t ask rats or mice if they are depressed. Instead, they use behavioral tests for classic depression symptoms such as anhedonia, the inability to take joy in pleasurable activities, Thompson says. Depressed animals “give up easily” in experiments that test their willingness to work for rewards like sugar water, or their interest in the intoxicating scent of a potential mate’s urine. “They can’t be bothered to cross the cage,” he says.Thompson and others have found that there are fewer connections, or synapses, between neurons that communicate reward signals in the brain in depressed animals. Other labs have found shriveled connections in neuronal circuits key to decision-making, attention and memory. Brain imaging studies in people with depression have also revealed abnormal activity in neural circuits that regulate emotion, suggesting that the findings in rodents may also apply to humans.If faulty neural connections are to blame for depression, the next question is, “How do we get atrophied neural pathways to regrow?” Krystal says.Circuit trainingThe answer, many scientists now believe, is the brain’s most abundant neurotransmitter, glutamate.Glutamate is the workhorse of the brain. It relays fleeting thoughts and feelings, and enables the formation of memories by strengthening synaptic connections. Glutamate is the reason you can still ride a bike years after you learned, even if you never practiced.Not all glutamate activity is good. Too much can cause the equivalent of an electrical storm in the brain — a seizure — and chronically high levels may lead to dementia. Abnormalities in glutamate receptors — specialized proteins on the surface of brain cells where glutamate can dock and bind — are linked to a wide array of psychiatric diseases, including depression and schizophrenia.To maintain balance, cells called inhibitory interneurons act like brakes, releasing a neurotransmitter called GABA that quiets brain activity. Most mind-altering drugs work by changing the balance between GABA and glutamate — amphetamines and PCP enhance glutamate signaling, for example, while alcohol inhibits glutamate and boosts GABA.By the 1990s, scientists had discovered that ketamine triggers a gush of glutamate in the brain’s prefrontal cortex. This region governs attention and plays an important role in emotional regulation. The out-of-body sensations that some people experience when they take ketamine may occur because this rapid release of glutamate “excites the heck out of a whole bunch of neurons” in the prefrontal cortex, says Bita Moghaddam, a neuroscientist at Oregon Health & Science University who discovered the drug’s glutamate-revving effect on rats while studying schizophrenia.Scientists aren’t sure yet how ketamine forms stronger neural circuits. But the hypothesis goes roughly like this: When ketamine enters the brain, it causes a short-term burst of neuronal activity that triggers a series of biochemical reactions that create stronger, more plentiful synaptic connections between brain cells.At first, many researchers thought ketamine’s antidepressant effects relied on a structure located on the surface of neurons, called the NMDA receptor. Like a key that fits into different locks, ketamine can bind to several types of NMDA receptor, making neurons release the excitatory glutamate neurotransmitter.This hypothesis suffered a blow, however, when several drugs designed to bind to the NMDA receptor (as ketamine does) failed in clinical trials for depression.Esketamine also complicates the story. Ketamine is made up of two molecules that form mirror images of each other, R- and S-ketamine. Esketamine is made up of just the S form and binds roughly four times as effectively as R-ketamine to the NMDA receptor. Despite acting much more powerfully on the NMDA receptor, studies in rodents suggest that S-ketamine is a less potent antidepressant than R-ketamine, although it’s not yet clear whether or not R-ketamine could work better in humans.Zarate and others now believe ketamine may work through a different receptor that binds glutamate, called AMPA. By pinpointing which receptor ketamine acts on, researchers hope to develop a similar drug with fewer side effects. One hot lead is a compound called hydroxynorketamine (HNK) — a metabolic byproduct of ketamine that does not affect NMDA receptors but still produces rapid antidepressant effects in rodents. The drug appears to lack ketamine’s disorienting side effects, and Zarate and Gould plan to launch the first small clinical trials to establish HNK’s safety in humans this year, likely in around 70 people. “I think we have a very good drug candidate,” Gould says. (Zarate and Gould, among others, have disclosed that they are listed on patents for HNK, so they stand to share in any future royalties received by their employers.)Plastic synaptic remodelersTo alter how the brain processes mood, scientists believe ketamine must ultimately change synapses. In experiments in rodents, Ron Duman of Yale University has shown that both ketamine and HNK can harness one of the brain’s most important tools for synaptic remodeling: brain-derived neurotrophic factor, or BDNF.BDNF is a protein intimately involved in shaping synapses during brain development and throughout the lifespan. Healthy brain function depends on having just the right amount of BDNF in the right place at the right time. Many mental illnesses, including depression, are associated with low or abnormal amounts of the protein. For example, samples of brain tissue from people who have died by suicide often contain abnormally low amounts of BDNF.Duman and colleagues have found that both ketamine and HNK cause a sharp uptick in the amount of BDNF that is released from neurons. This increase is required for the drugs’ antidepressant effects, and for the increase in dendritic spines — the stubby protrusions that form synaptic connections with other neurons. Both ketamine and HNK also seem to reduce inflammation, which has been linked repeatedly to the stress-induced loss of synapses.Ketamine is not the only compound that can induce rapid synaptic plasticity: Other psychedelics, such as ecstasy (MDMA), acid (LSD), and DMT also trigger similar structural changes in neurons and rapid antidepressant effects in rodents, researchers at the University of California at Davis recently found. The effects don’t hinge on getting high, the team reported in March in ACS Chemical Neuroscience. Even very small doses — too low to cause perceptual distortions — can increase synapse density and lift depression.Traditional antidepressants such as Prozac also increase BDNF levels in the brain, but not nearly as fast as ketamine does, Duman says. That is why most antidepressants take so long to remodel synapses and relieve depression symptoms, he says. Dissecting depressionBeyond promising new treatments, Zarate and other researchers see ketamine as a powerful tool for probing depression’s tangled neurobiology. Studies in mice and rats are a good start, but scientists need to study the drug in people to truly understand how ketamine affects the brain. Unlike traditional, slower-acting antidepressants, ketamine lends itself to short-term lab experiments.Zarate is using neuroimaging tools such as fMRI to study the human brain on ketamine. Past studies have shown that in people with depression, communication among several key brain networks is disrupted. One network, called the default-mode network (DMN), is involved in self-referential thoughts such as ruminating about one’s problems or flaws. This network tends to be hyperactive in people with depression, and less connected to more outwardly attuned brain networks such as the salience network, which helps the brain notice and respond to its surroundings.In one recent study, Zarate and his colleagues found that after receiving an IV dose of ketamine, people with depression had more normal activity in the default mode network, and that it was better connected to the salience network. At least temporarily, the drug seems to help people get unstuck from patterns of brain activity associated with repetitive, negative thoughts. Zarate does caution that the study results need to be replicated.The team has also used brain imaging to study how ketamine affects suicidal thoughts. About four hours after an infusion of ketamine, a chunk of the prefrontal cortex that is hyperactive in people with depression had calmed down, researchers found, which correlated with people reporting fewer thoughts of suicide.Ketamine also seems to tune other brain regions that are key to effective treatment. Last year, scientists published a study in mice showing that ketamine quiets abnormal activity in the lateral habenula, a small nodule wedged deep under the cortex. Some researchers have described the lateral habenula as the brain’s “disappointment center.” The region is responsible for learning from negative experiences, and is hyperactive in people with depression, as if “broadcasting negative feelings and thoughts,” Thompson says.Such studies remain exploratory. As to why ketamine works — and just as important, why its effects are transient — scientists are still speculating. “I think ketamine is resetting neural circuits in a way that improves the symptoms of depression, but the risk factors — whether genetic, environmental or other risk factors — are still present,” Gould says. “It seems to help reset things temporarily, but the underlying cause is not necessarily resolved.”Helen Mayberg, a neurologist at Mount Sinai Hospital in New York who specializes in using an experimental procedure called deep brain stimulation to treat depression, suggests that ketamine may be like using a defibrillator on someone experiencing cardiac arrhythmia. “I am not addressing the fact that you have underlying heart disease, but now that your arrhythmia is gone, I can concentrate on other treatments.”It’s important to put the potential risks of ketamine into perspective, particularly for people contemplating suicide, researchers emphasize. Most people are willing to tolerate severe side effects for other life-saving treatments, such as cancer drugs, Mayberg points out. “If you can interrupt an extreme suicidal plan and ideation, I’ll take that.”Ketamine in teens?For Krystal, weighing ketamine’s still largely uncharted risks and potential rewards ultimately comes down to a deeply personal question: “What would we want for ourselves? For our families? Do we want them to have to go through several failed trials over several months, or even a year, before taking a medication that might make their depression better in 24 hours?”Some of the hardest decisions are likely to involve children and adolescents. Hospitalization for youth suicide attempts and ideation nearly doubled between 2008 and 2015, leaving many clinicians — and parents — desperate for more effective and rapid treatments. Left untreated, depression is “really bad for the brain” and can cause serious, long-term cognitive and developmental problems when it starts young, Zarate says. “The question is, is that going to be better than the long-term side effects of ketamine?”Untreated depression is really bad for the brain, especially in the young. The question is, is that going to be better than the long-term side effects of ketamine?Scientists don’t yet know. Ketamine has been deemed safe to use as an anesthetic in children, but there aren't yet sufficient clinical data to show how low, repeated doses of ketamine used for depression could affect the developing brain.On a more fundamental level, scientists don’t fully understand the neurobiology of adolescent depression, notes psychiatrist Kathryn Cullen of the University of Minnesota. It may involve abnormalities in brain development, such as the way the prefrontal cortex connects to brain regions that process emotion, but “we don’t know if the brain connection abnormalities emerge because of toxic stress induced by depression, or if these abnormalities predispose people to develop depression, or if depression itself reflects abnormal development,” Cullen says. “It’s critical to figure out how to alleviate the biological changes that are associated with [teen] depression so that the brain can get back on a healthy trajectory.”Two recent clinical trials — one at Yale and another at Minnesota run by Cullen — have found that ketamine can lower symptoms in severely depressed teenagers, but neither study was set up to follow the teenagers long-term, says Cullen. Janssen is currently running a trial of its esketamine nasal spray with 145 youths who are suicidal, but the results of that study have not been published yet. Cullen thinks ketamine has potential for use in teens, particularly to avoid suicide, but “there are still a lot of unknowns.”Not just a quick fixWorldwide, depression afflicts more than 300 million people, making it the leading global cause of disability. When contemplating such overwhelming misery, the vision of a world in which depression can be cured with a single injection or squirt of nasal spray holds obvious appeal.But — despite the hype — that is not what ketamine offers, Bennett says. Based on her own experience as a patient, and her clinical work, she is troubled by the framing of ketamine as a “rapid” depression treatment if that precludes the slower, more effortful process of psychotherapy. Without psychotherapy, she says, “you’re not giving patients any tools to help themselves, just making them dependent on a molecule that has temporary effects. When the effect wears off, they have to go back for more medicine. This is going to be lucrative for the pharmaceutical company but probably not in the patient’s best interest.”In Bennett’s clinic, ketamine is administered only alongside talk therapy, which she uses to prepare patients before they take ketamine, and afterward to help them process the experience. “I think this is the only ethical way” to administer a drug that can trigger disorienting psychedelic experiences, she says. “This isn’t a ‘take two and call me in the morning’ situation.”There’s growing scientific interest in whether ketamine can enhance the effectiveness of therapy by increasing the brain’s ability to remodel circuits through experience, Krystal notes. And in 2017 a small Yale study found that providing cognitive behavioral therapy in tandem with ketamine can extend the drug’s antidepressant effects.Unlike some researchers and pharmaceutical companies, which consider ketamine’s and esketamine’s hallucinogenic side effects inherently negative, Bennett thinks that for some people the visions can be positive — particularly in the context of therapy. There’s scant scientific evidence to support the idea that such hallucinations are therapeutic, and they can be deeply disturbing for some people. (If people who experience hallucinations do better, it may simply be because they have received a higher dose of ketamine, Krystal points out.)Still, Bennett thinks researchers and clinicians need to stay open-minded about why ketamine is helping people — and be more attentive to the settings in which ketamine and esketamine are administered. “People consistently report that they experience the presence of God, or their own sacredness,” she says. “When someone comes to my office wanting to kill themselves, ready to die — and then they have a transformational moment where they believe their life is sacred — it’s indescribable how exciting that is as a clinician.”10.1146/knowable-032819-1 Emily Underwood is a freelance science writer and contributing correspondent for Science magazine. She is based in Coloma, California. Email: emily.l.underwood@gmail.com. Twitter: @em_underwood.This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.
How it Works - Yuletide EditionAdmitted we were powerless over the string of Christmas lights with three dead bulbs, mom’s green bean casserole and Aunt Barb’s warbling operatic rendition of O Holy Night.Came to believe that a power greater than us would deliver a brand new Toyota Tundra into the driveway in the morning.Made a decision to turn our will and our lives over to Amazon Prime next day delivery because we forgot that Uncle Dan was flying in on the Red Eye with his 5 kids.Made a searching and fearless inventory of our childhood bedrooms looking for proof that the 80’s really did happen even though we can’t remember.Admitted to anyone within earshot that we baked weed into the brownies we brought for Christmas dinner two years before.Were entirely ready to remove all the defects of character in every person seated at the table; by force if necessary.Humbly asked dad to remove the shortcomings in our bank account with a big fat Christmas check.Made a list of all the relatives who were going to ask “why aren’t you drinking?” and became willing to tell them to fuck off.Made direct deposits into the accounts of every family member from whom we had stolen money in the past; except when to do so would leave us short on rent.Continued to take inventory and when we found our hidden stash of coke from 12 years ago, promptly flushed it down the toilet.Sought through chocolate and the Hallmark Channel to improve our overall Christmas spirit as we understand it.Having survived the family Christmas still sober, we rushed home to our cats and our Darjeeling tea before remembering the world’s favorite drinking holiday is just seven days away.Happy holidays!
Dr. Adie Wilson-Poe was a straight edge kid. She grew up in Arizona then moved to the northwest at 19--first to Seattle and later to Portland--and found her home there. She wasn’t into drugs or drug culture; she was a punk rock kid who moved to Seattle for the music and ended up in science. While getting her psychology degree, Dr. Wilson-Poe became interested in drug use and addiction. She started studying neuroscience, specifically the neurobiology of psychology. The first time Dr. Wilson-Poe smoked weed, she was 25 and well into grad school. Although at the time there was scant scientific literature about marijuana, she studied whatever data she could find and came to understand that cannabis had medicinal properties. She also started studying the basic mechanisms of addiction and how different drugs affect the brain in unique ways. Dr. Wilson-Poe is an accomplished neuroscientist whose work is regularly funded by the National Institute on Drug Abuse.Why do you think so many pain-relieving drugs are addictive and what does the future hold in terms of cannabis-based pain relief?The whole reason that most people are using opioids or cannabinoids is because they're trying to relieve pain. There is a very complex interaction between pain relieving drugs that are also addictive. That dynamic interaction between pain relief and drug abuse or drug misuse is something that we spent a lot of time working on. There's a big gap between what we do in the lab and what we would do in the clinic and I'm trying to narrow that gap for cannabis and opioid interaction. We know that inhalation is a very common method that people use to relieve pain. We know it's a very effective method for relieving immediate pain. Oral products and edibles are great for nighttime when you can wait for them to kick in and then work overnight. But for relief when you're in pain, you need something that works right away, and we know that the lungs are a great method of doing that.How do you think cannabis can solve the opioid epidemic?Of all the things that cannabis can potentially do for humankind, the impact on the opioid crisis is by far the best and biggest thing it could do for humanity. There are a number of places where cannabis can interact with opioids. If we just follow one person, let's say you get injured at work, you throw out your back, and you have pain. You have a choice at the time that you're experiencing pain. You could start using cannabis right away and never even use an opioid at all. All of the side effects, all of the risks, all of the dependence potential. You can prevent it entirely by managing pain with cannabis. Cannabis has been used for pain relief on this planet for 5,000 years. The other thing we know from the evidence and my work has contributed to this as well, is that when they are used together, cannabis and opioids provide synergistic pain relief. So synergy means greater than additive effects. Rather than two plus two equals four you have two plus two equals seven or something. We know that this is a very robust effect, we see it in people, we see it in all other mammals, we see it whether you use a synthetic cannabinoid or delta-9, you see it whether you use codeine and morphine. When you use the drugs together, you get better pain relief and what that means--the outcome of that better pain relief--is that you don't need as many opioids.Can you explain how cannabis can also be used for addiction treatment?Let's say again: you have your injury on the job and your doctor prescribed opioids. You took them as directed and get to a point where your injury has resolved, but now you're physically dependent on opioids. There's a role for cannabis here. Part of the science is a little bit more messy than the others, but there’s some preliminary results showing that people who are physically dependent on opioids have some withdrawal relief from cannabis. During withdrawal you feel restless, you can't sleep, you’re irritable. Those symptoms are very well treated with cannabis. People have always talked about weed as a gateway drug, but now we’re hearing that marijuana is the exit drug. What are your thoughts?The gateway hypothesis came out of some evidence that was produced in the 70s, 80s, and 90s, which showed that there’s a correlation between using cannabis and using harder drugs like opioids. But that correlation is also true for people who use nicotine and alcohol. Just because those things are correlated with the use of harder drugs doesn't mean that they cause a person to use harder drugs. That gateway hypothesis has been thoroughly refuted in more recent work. We now know that cannabis is not necessarily the gateway to causing someone to use other drugs. We're in this new time where we see that cannabis is not the gateway drug to opioid use, but rather it’s an important tool for exiting from dependence on opioids.How has our government ignored the evidence that cannabis is less dangerous than alcohol? In the early seventies, President Nixon assigned a bunch of scientists and doctors the task of analyzing cannabis’ effects on people and making a determination about how safe or how dangerous it was. This was the Shafer Commission. They wrote up this exhaustive report and gave it back to him. The report said, "This is a very innocuous substance, it shouldn't be regulated, it's even less dangerous than alcohol." But Nixon ignored the evidence and allowed cannabis to persist as a schedule one drug.Through the history of prohibition there’s been a blatant disregard of the evidence. We saw this even as recent as the current administration. Jeff Sessions is probably the worst at this. Everything that comes out of his mouth about cannabis is directly in contradiction to the evidence. The evidence has always been there to support cannabis as a relatively safe substance, especially compared to other drugs.Can you talk about what you're doing with the business Smart Cannabis? We're really interested in what the effects of cannabis in people are and how we can use that information to both better support the people using cannabis and help to support the people who are cultivating or producing cannabis. We have to study it in people and ask them, how did this make you feel? Knowing what people actually find enjoyable, not just intoxicating because there's really a difference there, right? Like just because something has 30% THC and it got you really high doesn't mean that was necessarily an enjoyable experience. Maybe you’d have a better time on Friday night if you had had a 17% flower, but we don't know that until we actually test it in people. Do you have an opinion on the recent vaping controversy?Oil cartridges are not going anywhere. This is an incredibly convenient and very popular way for people to consume cannabis. But what we really need to focus on is what’s the safest possible way to consume. Propylene Glycol and Vitamin E Acetate are probably never going to be allowed to be in these cartridges again. Obviously, all of these flavors and additives that break down into really nasty chemicals, those are going to be outlawed. We're going to need to have some regulation around.We're probably going to see some change in the technology also. You can't have a battery that's over this amount of voltage. You can't have a ceramic coil or a fiberglass coil that gets hotter than this temperature, because we know at that temperature, that's when things start to break down and even if we don't have the FDA or some other regulators telling us that this is what we need to do, it's on us, it's on the industry to be able to make those decisions for the health of our consumers.Cannabis events help to educate people about cannabis, what do you see as your role in all this?I feel incredibly grateful that this is what I get to do with my time on planet earth. It just so happened that legalization and the opioid crisis was happening when I was going to grad school. I get to participate in something that could leave a very long-lasting mark on humanity. It's also interesting that a lot of my colleagues--a lot of doctors, a lot of healthcare professionals--because of the federal prohibition, there’s a lot of conservative thinking. There are a lot of people who are afraid to talk with their patients about cannabis or a lot of people who are afraid to speak about these things in public. I believe in doing no harm and it’s very clear to me from the evidence that cannabis is a medicine and opioids, although useful for certain things, are dangerous. I feel very privileged that I get to participate in these really important conversations at a really important time. But one component of that is my not fearing what the National Institutes of Health are going to do or what the DEA is going to do. There’s some inherent risk for me in openly talking about these kinds of ideas because so many of my colleagues would just rather hide in the laboratory because it's too much of a risk for them. But the right thing to do is to reduce harm and keep people alive and I feel very privileged that I get to play some part in that.
“I could sure use a drink.”It’s a popular saying, an easy way to blow off steam after a stressful day or week. But for people in recovery, dealing with stress isn’t as simple as turning to alcohol (or drugs) for substance-infused relaxation. Once you’re living sober, there’s no easy way to mask your stress. Instead, you have to deal with it head-on. Unexpected emergencies or events, like the ongoing wildfires that are devastating California, can really challenge your recovery, no matter how long you’ve been sober. Personal tragedies or challenges can have the same affect. However, your recovery experience can also be a source of strength. The lessons you’ve learned in sobriety can help you get through other dire situations. With that, you can also help others. Here are some tips for staying sober, even when life is throwing curveballs. Be Honest About What’s in Your ControlMost people in recovery are familiar with the serenity prayer: “God grant me the serenity to accept the things I cannot change, Courage to change the things I can, And wisdom to know the difference.”No matter what your higher power, the lessons in this prayer are important throughout recovery, especially in time of stress. When you’re dealing with an unexpected event, take a moment to decide what’s in your control. You might feel better after packing an emergency bag if fires are near your area, for example. Exerting control where you can is empowering. However, what’s even more important is to remember what you cannot control. Trying to manage things that are uncontrollable, like hoping the fires do not come your way, can be exhausting and frustrating. It’s best to acknowledge where your limits are, and not waste time on things beyond your control. Lean Into Your Recovery CommunityIf you’re living sober, you can’t unwind with a drink at the end of the day. However, you can do something much healthier: go to a meeting, or go for a walk with someone who is also in recovery. Having open conversations about your fears and worries can help you process them, rather than just masking them with a chemical high. This can be especially helpful when you’re dealing with a local disaster. Most 12-step meeting are hyper local. That means that many people in your meeting are dealing with similar anxieties and fears, and can understand what you’re going through. Plus, they’ll understand navigating difficulties while dealing with the day-to-day of life in recovery. Watch for Relapse SignsAny time you’re dealing with increased stress, you are more at-risk for relapse. That’s why it’s important to be self-aware during times when you’re dealing with the unexpected. Be on the lookout for relapse warning signs that indicate that you’re struggling in recovery. For example, you might stop going to meetings, or start spending more time with the people who are unhealthy for you. If you notice that your recovery is faltering, reach out for help. Talking to a sponsor or trusted friend can help you get back on track before you really slip up. And, if you do end up using, remember that relapse is a normal part of recovery. The important part is getting help to get back on track as soon as possible. Remember, You Are ResilientIn recovery, we’re told to take things one day at a time. This is good advice for dealing with unexpected emergencies as well. Sometimes, when it seems like you can’t go on because of stress of uncertainty, remember that you just have to get through today. Everything is much more manageable when you’re only thinking about the next 24 hours. That’s one lesson that recovery has taught you, but the truth is that your whole recovery experience can fortify you in trying times. You’ve already overcome the odds and changed your life. You now know from experience that you can cope with whatever comes your way: even if it seems entirely overwhelming right now. Asana Recovery offers residential and outpatient treatment in Costa Mesa, California. Learn more by calling 949-438-4504.
By Jenn Abelson, Aaron Williams, Andrew Ba Tran, Meryl Kornfield, Investigative Reporting WorkshopAt the height of the opioid epidemic, Walgreens handled nearly one out of every five oxycodone and hydrocodone pills shipped to pharmacies across America.Walgreens dominated the nation’s retail opioid market from 2006 through 2012, buying about 13 billion pills — 3 billion more than CVS, its closest competitor, according to a Drug Enforcement Administration database of opioid shipments. Over those years, Walgreens more than doubled its purchases of oxycodone.The company had “runaway growth” of oxycodone sales because it continued to send pills to stores “without limit or review,” Edward Bratton, Walgreens manager of pharmaceutical integrity, wrote to another employee in 2013. The email is among thousands of documents recently disclosed in a federal lawsuit that seeks to hold Walgreens and other businesses responsible for the nation’s opioid crisis.While most chain and independent pharmacies relied heavily on wholesalers to supply their prescription opioids, Walgreens obtained 97 percent of its pain pills directly from drug manufacturers, a Washington Post analysis of the data shows. This arrangement allowed Walgreens to have more control over how many pain pills it sent to its stores.By acting as its own distributor, Walgreens took on the responsibility of alerting the DEA to suspicious orders by its own pharmacies and stopping those shipments. Instead, about 2,400 cities and counties nationwide allege that Walgreens failed to report signs of diversion and incentivized pharmacists with bonuses to fill more prescriptions of highly addictive opioids.From 2006 through 2012, Walgreens ordered 31 percent more oxycodone and hydrocodone pills per store on average than CVS pharmacies, and 73 percent more than other pharmacies nationwide, according to The Post’s analysis of the DEA database, known as the Automation of Reports and Consolidated Orders System (ARCOS).When Walgreens considered surveying its pharmacies in Florida in 2011 to identify questionable pain pill customers, a company attorney advised caution: “If these are legitimate indicators of inappropriate prescriptions perhaps we should consider not documenting our own potential noncompliance,” according to an email disclosed in the case.In 2012, a drug distributor produced a report for Walgreens that flagged nearly half of the chain’s roughly 8,000 stores for dispensing high numbers of controlled substances, including oxycodone, court records show.After warnings from the DEA, Walgreens agreed in 2013 to pay $80 million — a record settlement for the agency at the time — to resolve allegations that the company failed to sufficiently report suspicious orders and negligently allowed controlled substances, such as oxycodone and other prescription pain medications, to be diverted for abuse and illegal black market sales.The large volume of pills flowing into Walgreens pharmacies made some stores targets for crime, including armed robberies and employee theft, according to police officials, board of pharmacy records and other published reports. In 2014, a pharmacy technician who stole about 25,000 pain pills from a Walgreens in Missouri told state investigators that another employee gave him instructions on how to pilfer the pills and sell them during breaks in the store bathroom and pharmacy parking lot.Now, Walgreens is one of the holdouts in the federal suit playing out in Cleveland after other major distributors and drug manufacturers reached a settlement with two Ohio counties on Oct. 21. The trial for Walgreens was postponed until next year. CVS and other major pharmacy chains are also defendants.“Because Walgreens had full visibility into all dispensing related information necessary to reveal red flags and criteria of suspicion, Walgreens might even be viewed as more culpable due to the wealth [of] data at its complete disposal,” the plaintiffs allege.“Walgreens might even be viewed as more culpable due to the wealth [of] data at its complete disposal.”The company denied that it incentivized pharmacists to inappropriately fill prescriptions and defended its practices in statements.“Walgreens is completely unlike the wholesalers involved in the national opioid litigation. We never sold opioid medications to pain clinics, internet pharmacies or the ‘pill mills’ that fueled the national opioid crisis,” the company said. “We never marketed or promoted opioid medications.”Walgreens also said the pain pill data is “misleading” because the records are seven years old and the chain stopped the internal distribution of controlled substances to its pharmacies in 2014.Employees were “incredibly diligent and careful” to ensure that pharmacies were not involved in diversion, the company said. “We proudly stand by our pharmacy professionals and their record of professional judgment and patient care.”A Directed Effort’ To Increase SalesWalgreens traces its roots to 1901, when Charles Walgreen Sr. pulled together enough money for a down payment on the pharmacy where he worked on Chicago’s South Side. He shook up the business by adding more merchandise and making some of the drugs himself to keep prices low.His model was successful, and over the next two decades he opened about 20 stores. Today, the company operates 9,277 pharmacies in all 50 states and the District of Columbia.As the demand for opioids increased in the early 2000s, Walgreens expanded its internal distribution network. The company added two facilities in Ohio and Florida that had special security to handle controlled substances, including oxycodone. It was an advantage over CVS, which relied entirely on outside suppliers for the medication.In 2006, though, regulators found problems with Walgreens’s distribution network. In May of that year, the DEA sent the company a letter detailing record-keeping and security deficiencies that the agency discovered during an investigation at the Walgreens facility in Perrysburg, Ohio, according to documents filed in the Cleveland court case.The DEA said Walgreens had an “insufficient” system for reporting suspicious orders of controlled substances. At the time, Walgreens identified questionable orders by analyzing the average daily prescriptions filled by stores in groups of 25, an internal memo shows. The DEA told the company that the size, pattern and frequency of orders should instead be used to flag suspicious ones.Two years later, Walgreens conducted an internal audit of its Perrysburg facility and discovered officials there had not properly overhauled the suspicious-order system to comply with the DEA. The audit, filed in court, noted this was an issue at all company distribution centers and “should be addressed to avoid potential DEA sanctions.”In 2009, Walgreens began testing a new method at several stores that identified suspicious orders based on order size and frequency. But an internal company document filed in court stated that Walgreens was “capturing data but not cutting orders.”As the opioid crisis deepened, the DEA stepped up enforcement against drug manufacturers, distributors and pharmacies. The agency again turned its attention to Walgreens and threatened in a 2009 letter to revoke the registration of a store in San Diego.A DEA investigation found that the San Diego store on Midway Drive had filled prescriptions issued by doctors who weren’t licensed in California. It also had dispensed prescriptions to people the pharmacy “knew or should have known were diverting the controlled substances,” agency enforcement records show. One customer over seven months obtained prescriptions for hydrocodone issued by four Florida physicians — an indication that she was “doctor-shopping” to procure pain pills, the DEA record shows.In April 2011, Walgreens entered into an agreement with the DEA to settle the case. The company promised to maintain a program to detect and prevent diversion of controlled substances from its stores across the country.The DEA would later discover that Walgreens had been engaged in “a directed effort to increase oxycodone sales,” agency records show. In a July 29, 2010, email, Walgreens sent out a spreadsheet to managers ranking all Florida pharmacies on their oxycodone dispensing with the instruction to “look at the stores on the bottom end . . . We need to make sure we aren’t turning legitimate scripts away.”Meanwhile, changes in the state’s laws over the years had shifted sales of prescription opioids from pain clinics to pharmacies. Soon the chain was grappling with a surge of pain pill customers in Florida.Kristine Atwell, who managed distribution of controlled substances at Walgreens’s Jupiter facility, had emailed corporate headquarters urging that stores justify their large volumes, including one pharmacy that ordered 3,271 bottles of oxycodone in a 40-day period.“I don’t know how they can even house this many bottle(s) to be honest,” Atwell wrote in early 2011 in an email previously reported on in The Post.A few months later, Walgreens decided to review the “significant increase” in controlled substance prescriptions in Florida, according to company emails filed in court.As part of its broader business initiative called “Florida Focus on Profit,” Walgreens officials discussed surveying some of its pharmacies. The proposed questions included, “Do pain management clinic patients come all at once or in a steady stream?” and “Do you see an increase in pain management prescriptions on the day the warehouse order is received?”But Dwayne Pinon, a Walgreens attorney, warned against “documenting our own potential noncompliance” and the questions were dropped from the survey, court records show. Pinon, through a company spokesman, declined to comment.Walgreens eventually renamed the survey effort “Focus on Compliance” after an employee in an email questioned the “Focus on Profit” title.For the first half of 2011, Walgreens accounted for 100 of the top 300 pharmacies in oxycodone purchases in Florida, and some of these company stores bought more than double the average amount of the opioid obtained by other pharmacies in the state, according to DEA enforcement records.For the first half of 2011, Walgreens accounted for 100 of the top 300 pharmacies in oxycodone purchases in Florida.Agency investigators met with Walgreens officials that August to express concerns about the high volume of pills. In advance of the meeting, Walgreens sent a disc to the DEA with a file labeled “suspicious drug” orders.“This gobbledygook is impossible to read and I stopped printing it when it reached 2” [inches] thick,” a DEA investigator wrote in an email to her colleagues after the meeting. “Obviously this is unacceptable.”Days after the DEA meeting, Walgreens devised a plan to restrict a store in Hudson, Fla., to a monthly 100 bottles of 30-milligram oxycodone, one of the most coveted pain pills on the black market because of its potency, according to DEA enforcement records. But the pharmacy routinely exceeded the limit, procuring 331 bottles in September 2011, 371 bottles in October, 200 bottles in November and 263 bottles in December, DEA enforcement records show.Some Walgreens stores attracted so many pain pill customers that the pharmacies had to hire security or call the police.In Oviedo, Fla., large crowds began waiting for the Walgreens on Lockwood Boulevard to open. Between August 2010 and November 2011, Oviedo police responded to 17 incidents at that location, arresting 35 people for charges related to controlled substances.Oviedo Police Chief Jeffrey Chudnow wrote dozens of letters and contacted Walgreens’s chairman and chief executive in March 2011 to plead for help and let them know the pharmacy parking lots at two company stores in the city had “become a bastion of illegal drug sales and drug use.”Chudnow, who has since retired, told The Post that he never received a response.The Lockwood Boulevard store doubled the number of 30-milligram oxycodone pills it ordered from 73,300 in March 2011 to 145,400 pills in July 2011, according to the DEA data. The Post and HD Media, which publishes the Charleston Gazette-Mail in West Virginia, fought a year-long legal battle for access to the DEA database.Nationwide, the explosion in pain pills helped fuel crime. Armed robberies spiked at independent and chain pharmacies. Some stores were repeatedly targeted.In Michigan, a Walgreens pharmacist purchased a gun to protect himself after the company refused to improve security following a 2007 robbery, the pharmacist alleged in a lawsuit. In 2011, the pharmacist shot at two masked gunmen during a robbery attempt on an overnight shift. No one was harmed, but the pharmacist was fired and sued Walgreens.Later that year, an armed gunman who fled after demanding painkillers at a Walgreens in Tennessee prompted a lockdown at nearby schools, according to police. In Colorado Springs, robbers hit multiple Walgreens pharmacies 14 times in 2011 and seven times in February 2012.Gaps in the SystemAs pharmacy robberies made headlines, the DEA escalated its investigation of Walgreens. The agency served warrants on six stores scattered across Florida and the Jupiter distribution center in spring 2012.Walgreens responded by slashing shipments of opioids to the six stores. In the event of the DEA shutting down the Jupiter location, the chain planned to shift distribution to outside suppliers and its Perrysburg, Ohio, facility, the same one the DEA had cited in 2006, according to company emails filed in the court case.During a meeting with the DEA, Walgreens told the agency it wanted to “cooperate and avoid litigation,” as stated in an internal company presentation from July 2012.Walgreens officials detailed steps the chain was taking to address the DEA’s concerns, including updated training for pharmacists to identify suspicious prescriptions. The company said while its suspicious-order monitoring program “did not automatically halt suspicious orders upon identifying them, it did systematically decrease [controlled substance] order quantities if the quantity ordered exceeded certain thresholds.”Later that summer, DEA investigators interviewed pharmacists at Walgreens stores in Fort Pierce, Fla.The DEA found that one of the pharmacists had filled at least seven oxycodone prescriptions issued by a Miami gynecologist, ignoring warnings other employees had left about the doctor in pharmacy records, including: “FAKE CII DO NOT FILL ANY CII CANDY DR.”The note referred to doctors who appeared to be writing bogus prescriptions for substances listed on Schedule II of the Controlled Substances Act.Questioned by the DEA about the prescriptions, the pharmacist said, “We should not have filled them,” according to agency enforcement records.In September 2012, the DEA employed its most severe enforcement action: Agents padlocked a vault containing oxycodone and other controlled substances at the Walgreens distribution center in Jupiter and later threatened to revoke the registrations of the six pharmacies.Walgreens responded by launching a task force and discussing ways to tighten up oversight of opioids distributed to its stores.When pharmacies hit limits imposed by Walgreens, they could still transfer pills from other stores or order from outside suppliers, court records show. Pharmacies could also find workarounds by placing special PDQ orders, meaning “pretty darn quick,” from Walgreens internal network.The company proposed eliminating PDQ orders for oxycodone, but Kermit Crawford, then a top executive at Walgreens who oversaw the pharmacy business, objected to the change.“I was not under the impression this was a done deal. Concerned we are ‘all or none,’ ” Crawford wrote in an Oct. 1, 2012, email disclosed in the case. “We have to do what’s right for patients also.”Crawford, who later became president and chief operating officer of the Rite Aid chain, declined to comment.At the same time, Walgreens wrestled with other gaps in the system.In October 2012, a Walgreens pharmacy in Modesto, Calif., came under scrutiny because it was purchasing about 17,500 pills containing hydrocodone per week, putting the drugstore “over the corporate limit” of the number of pills it was permitted to order, according to a company email cited in court records.To obtain more hydrocodone, the Modesto pharmacy, on McHenry Avenue, ordered pills from the distributor Cardinal Health, the document noted. When that set off red flags at Cardinal Health, the store transferred opioids from nearby Walgreens pharmacies, procuring so many pills that it led to shortages at the other stores.Walgreens conducted an investigation and discovered “employee pilferage” and fired an employee, company emails filed in court show. The Modesto pharmacy also stopped filling prescriptions from two local doctors.Cardinal Health, which had paid a $34 million fine in 2008 to settle allegations that it failed to report suspicious orders, declined to answer questions about the Modesto orders and said, “We are proud of our rigorous analytics system, including conservative, customer-specific thresholds, that we use to spot, stop, and report to our regulators any opioid order that is suspicious.”The McHenry Avenue Walgreens was the single largest purchaser of pain pills in the entire Walgreens chain from 2006 through 2012, and one out of every five oxycodone pills ordered was a 30-milligram tablet, The Post’s analysis found. Robbers targeted the store five times for prescription opioids from 2016 through 2018, police said.Walgreens said demand for opioids at the pharmacy was driven by hospitals, surgery centers and other pain treatment facilities in the area.“Walgreens thoroughly investigated concerns regarding this Modesto pharmacy after Cardinal raised them,” Walgreens said in its statement. “We found that the pharmacy was fully complying with all applicable internal policies and procedures for filling prescriptions for controlled substances.”A Dramatic StepIn November 2012, drug distributor Anda analyzed nearly 1.3 billion pills, including oxycodone, handled by Walgreens. The review “flagged” 3,768 of the chain’s pharmacies for dispensing high numbers of controlled substances in all 50 states, as well as Puerto Rico and Washington, D.C., court records show. The report, filed with redactions, identified 226 of 253 stores in Arizona, 64 of 69 pharmacies in Oregon and all 14 stores in Maine.Drug manufacturer Teva Pharmaceutical, which owns Anda, declined to comment.Soon after, Walgreens launched a new division called pharmacy integrity. Tasha Polster, who had served on the company’s task force, was tapped to lead that effort. (Polster is not related to Judge Dan Aaron Polster, who is presiding over the federal lawsuit).In December 2012, Polster emailed Dan Doyle, a Walgreens finance executive, and said without elaborating that the DEA was alleging the company’s suspicious-order monitoring program was “inadequate.” The DEA, she wrote in the email recently disclosed in court, was “demanding civil penalties, potentially totaling hundreds of millions of dollars.”Polster requested a team of a dozen people to review controlled substance orders before Walgreens shipped the drugs to its pharmacies.“The Company has enhanced its suspicious order monitoring program for controlled substances in an effort to convince DEA that the proposed penalty is excessive and that our new processes will ensure that similar incidents do not recur,” Polster wrote.A Walgreens spokesman said Polster and Doyle, who still work for the company, declined to comment.By the end of 2012, Walgreens’s orders of pain pills containing oxycodone and hydrocodone dipped to 2.2 billion from its peak of 2.4 billion the previous year, ARCOS data shows.But the DEA continued to investigate. In February 2013, the agency served a warrant and inspected the Perrysburg distribution center.In response, Walgreens halted shipments of controlled substances from Perrysburg. It was a dramatic move that Walgreens hoped would “eliminate any immediate need for further DEA administrative action,” three lawyers representing Walgreens wrote in a Feb. 20, 2013, letter to DEA officials that was filed in the court case.At first, Walgreens turned to Cardinal Health to distribute controlled substances to its pharmacies. But Cardinal Health had “red flagged” 367 Walgreens stores and would not ship to them because “they are considered suspicious,” according to internal emails between Walgreens employees.Cardinal Health, one of the defendants that recently reached a settlement in the national opioid litigation, did not respond to questions about its refusal to send pills to these Walgreens pharmacies.Walgreens soon found another distribution partner, AmerisourceBergen. In March 2013, Walgreens announced a deal that gave it an ownership stake in AmerisourceBergen in exchange for a distribution agreement.As the DEA investigations pressed on, Walgreens stopped filling pharmacy orders for opioids that exceeded certain limits, according to company documents filed in court.This prompted pill shortages and irate customers who complained to a corporate hotline.In June 2013, a pharmacy manager in Greenville, N.C., emailed the pharmacy integrity division that she had run out of oxycodone a week earlier and told customers the drugs would arrive that day. When the pills didn’t show up, she wrote that “luckily” she found bottles at another local Walgreens, court records show.“I placed a PDQ order for oxycodone . . . (one bottle will NOT be sufficient) – please send us this order ASAP! We are losing business over this!”The next day, Steven Mills, with the pharmacy integrity division, responded that PDQs should be used only in “an emergency situation.”“You have to realize the reason why we have issues with the DEA today, is due the high amounts of Oxycodone distributions over the past 3 years,” Mills wrote back in an email. “We had to create limits to all stores which protects the integrity of the Pharmacist, DEA license, and the Walgreen Company as a whole.”Half of the pain pills ordered by the Greenville store were oxycodone — nearly twice the average of all other pharmacies across the country, according to The Post’s analysis of DEA data from 2006 through 2012. Police said robbers targeted the store earlier this year and stole prescription pills, including opioids.The company said the Greenville pharmacy’s orders “were a legitimate reflection of the demands caused by its particular location and market, and Walgreens is unaware of any diversion of prescription pain medication at that pharmacy.” Mills, who still works at Walgreens, declined to comment through a company spokesman.On June 11, 2013, the DEA announced Walgreens had agreed to pay an $80 million civil penalty to resolve federal allegations that the pharmacy chain failed to sufficiently report suspicious orders and that the failure was a “systematic practice that resulted in at least tens of thousands of violations,” records show.In a statement at the time of the settlement, Crawford, of Walgreens’s pharmacy division, said, “As the largest pharmacy chain in the U.S., we are fully committed to doing our part to prevent prescription drug abuse.”Under the agreement, Walgreens admitted that it failed to uphold its obligations under the law and agreed to surrender its DEA registration for the Jupiter distribution center and six stores in Florida until 2014. The settlement addressed the claims in Florida and resolved open civil investigations into Walgreens by U.S. attorneys in Colorado, Michigan and New York, as well as other DEA field offices nationwide.In Colorado, federal investigators had identified over 1,600 violations of the Controlled Substances Act at Walgreens stores, including fraudulent prescriptions and the dispensing of controlled substances to customers without a prescription, according to the U.S. attorney’s office in Colorado.Employee TheftWalgreens eventually stopped the internal distribution of oxycodone and hydrocodone, although the company continued to purchase controlled substances from outside suppliers. The chain also removed sales of opioids from its bonus calculations for pharmacists, according to court records.The company declined to explain the change, but said dispensing volume was “one of many factors” used to determine bonuses. “The nominal compensation factor in question in no way incentivized pharmacists to inappropriately fill prescriptions for any medication,” Walgreens said.Although Walgreens had imposed limits on the number of opioid pills pharmacies could order, stores could submit override requests if they needed more.During 2014 and 2015, the company approved more than 95 percent of these override requests from stores for controlled substances — totaling thousands of orders — and boosted its overall sales of oxycodone, according to an internal presentation filed in court.As the pain pills kept flowing, so did problems with diversion. In 2015, Walgreens reported to the DEA that nearly 2 million doses of controlled substances were stolen or lost — a 16 percent increase from the previous year, documents filed in court show.Employee theft accounted for the largest share of missing pills, nearly one-third, followed by armed robberies and “unexplained loss,” the documents say. Pills containing oxycodone and hydrocodone topped the list.Walgreens’s business practices have drawn scrutiny from state regulators, as well. The boards that license the individual stores and pharmacists have documented problems at company stores such as inadequate security, delays in reporting thefts, inaccurate audits of controlled substances and insufficient vetting of employees.In Missouri, Walgreens employees allegedly have pilfered at least 138,000 pills containing hydrocodone and oxycodone from 19 stores since 2005, according to state board records. One of these cases involved a pharmacy technician at Walgreens who stole about 7,500 pain pills in summer 2016 and told investigators that she knew “how easy it would be” to take handfuls of pills and evade security cameras.The Post examined 67 investigations in 12 states in which pharmacy boards censured Walgreens or placed pharmacies on probation for violating state regulations, including inadequate security and theft of drugs. In some instances, the company had to pay fines.In July, Walgreens agreed to pay a $335,000 fine after the California State Board of Pharmacy discovered that the company had allowed a woman without a pharmacy degree or license to dispense prescriptions for over a decade.The employee, Kim Thien Le, had worked at Walgreens since 1999, rising from pharmacy cashier to pharmacy manager in 2016. She used the license numbers of other pharmacists to dispense 745,355 prescriptions at 395 pharmacies, including some remotely. In all, Le filled more than 100,000 prescriptions for controlled substances, such as oxycodone, hydrocodone and fentanyl, according to state records.Le, who was charged this summer with three felonies alleging she falsely impersonated licensed pharmacists, has a court date in January. An attorney representing Le declined to comment.The fine paid by Walgreens is one of the largest in the board’s history.Walgreens declined to answer questions about Le and other enforcement actions.“We take great pride in the judgment and patient care of our 28,000 pharmacists,” the company said. “In the event of a rare and isolated instance when we learn of an employee acting improperly, we act swiftly to address the matter and cooperate fully with law enforcement.”This story was originally published by the Investigative Reporting Workshop, a nonprofit,  nonpartisan newsroom at the American University School of Communication.

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