In this new publication, the authors found that both counselor and program characteristics influence counselor attitudes towards use of medications in treating addiction. People who are looking for treatment need to ask about these attitudes prior to agreeing to enter a program or therapeutic relationship. It is a sign of how far the US treatment industry must go when "attitude" determines the treatment you get, rather than evidence based guidelines. And be skeptical when a program or staff member says they use "evidence based practices." Too often, that consists primarily of some training to update counseling skills, but it doesn't involve moving beyond an ideological approach to a scientific one. Consequently, too many treatment staff still see science as useful only insofar as it can validate already held assumptions. We all know, however, that's not how science works. It's designed to upset and surprise because it uses methods to minimize bias. And we're all biased, one way or another. Bottom line: people and families looking for treatment need to educate themselves about the scientific knowledge base of what addiction is and the most current methods available to treat it and then be prepared to ask the program or counselor about specific practices and then to look elsewhere if a program doesn't offer what they are looking for. Consumers can be a significant force in moving the industry forward.
MW
Addictive Behaviors
Volume 36, Issue 6, June 2011, Pages 576-583
Special Issue: Addiction Treatment: Evidence-Based Policy and Practice
Counselor attitudes toward the use of naltrexone in substance abuse treatment: A multi-level modeling approach.
Abraham AJ, Rieckmann T, McNulty T, Kovas AE, Roman PM.
Institute for Behavioral Research, Center for Research on Behavioral Health and Human Services Delivery, University of Georgia, 112 Barrow Hall, Athens, GA 30602, USA; Department of Sociology, University of Georgia, Athens, GA 30602, USA.
Abstract
Alcohol use disorders (AUDs) continue to be one of the most pervasive and costly of the substance use disorders (SUDs). Despite evidence of clinical effectiveness, adoption of medications for the treatment of AUDs is suboptimal. Low rates of AUD medication adoption have been explained by characteristics of both treatment organizations and individual counselor's attitudes and behaviors. However, few studies have simultaneously examined the impact of organizational-level and counselor-level characteristics on counselor perceptions of EBPs. To address this gap in the literature, we use data from a national sample of 1178 counselors employed in 209 privately funded treatment organizations to examine the effects of organizational and individual counselor characteristics on counselor attitudes toward tablet and injectable naltrexone. Results of hierarchical linear modeling (HLM) show that organizational characteristics (use of tablet/injectable naltrexone in the program, 12-step orientation) were associated with counselor perceptions of naltrexone. Net of organizational characteristics, several counselor level characteristics were associated with attitudes toward tablet and injectable naltrexone including gender, tenure in the field, recovery status, percentage of AUD patients, and receipt of medication-specific training. These findings reveal that counselor receptiveness toward naltrexone is shaped in part by the organizational context in which counselors are embedded.
Monday, April 18, 2011
Friday, April 15, 2011
Concise description of the neurobiology of addiction
In this Baltimore Sun article Dr. David Linden of Johns Hopkins University gives an unusually succinct description of the underlying neurobiology of the development of addiction. Note the interplay between genetics and intoxicant exposure: if you're brain isn't genetically vulnerable, you are not likely to become addicted to a particular drug. Note also that this vulnerability is substance-specific, not a generalized "addictive personality."
MW
Baltimore Sun
Johns Hopkins neuroscientist David Linden explains the biology of pleasure
With his new book, he seeks to find out why vices -- and even virtues -- can hold such sway over our lives
By Mary Carole McCauley, The Baltimore Sun
April 14, 2011
Not all addictions live up to their advance press.
In the past decade, it's become common to casually and humorously describe a favorite activity in the parlance of chemical dependency. People speak of being "addicted" to chocolate or high-fat foods, playing video games, buying expensive designer shoes, watching weekly episodes of "American Idol" to sleeping on high-thread-count sheets. But according to "The Compass of Pleasure," a new book by Johns Hopkins neuroscientist David Linden that is being released today by The Viking Press, just two of those pursuits -- eating fatty foods and shopping -- can become genuine addictions for some people. Watching television, playing World of Warcraft and swaddling yourself in Egyptian cotton probably cannot.
Who knew that feeling good could be so complicated?
"Addiction is defined by the changes that certain activities can make in the brain," Linden says.
"Basically, some activities have been shown to short-circuit the medial forebrain pleasure circuit. The process is the same, whether someone is taking crack cocaine or gambling or having risky sex or shopping. These morphological changes bring about a gradual transition from liking to wanting, and the result is compulsive behavior."
The vast majority of people who pursue habit-forming activities will never become compulsive. Our genes play a major role in determining who will become addicted, how badly and to what substance. It also generally takes repeated exposure for a harmful habit to develop.
For example, Linden points out that for even a drug as highly addictive as heroin, two of every three people who inject the narcotic directly into their veins don't become junkies.
In addition, some pursuits that may technically qualify as addictive carry positive benefits for individuals and society that vastly outweigh the potential harm, such as running a marathon, or an extended bout of contemplative prayer.
"Pleasure is our compass, no matter what we do," Linden says.
"But a philosophical question arises from these findings. If we catch a pleasure buzz from our noblest instincts, does that make them less noble?"
Conversely, just because a substance doesn't create a physical dependency doesn't mean it's safe. LSD might not activate the medial forebrain, but someone who drops acid and jumps off the roof because he thinks he can fly is likely to get hurt.
"There's a whole bunch of risk-taking behaviors that aren't addictive," Linden says. "We're motivated by reasons other than seeking pleasure."
Addiction, he says, is just one form of learning. The changes that occur inside the brain when someone studies calculus are nearly identical to the changes that occurs when he smokes crack.
As Linden explains it, when human beings bliss out by watching a sunset, getting a back rub or drinking a glass of red wine, the ventral tegmental area in our brains is releasing a neurotransmitter called dopamine that is getting picked up by a nearby bundle of neurons called the nucleus accumbens.
Under normal circumstances, pleasure flows and ebbs; dopamine gets released and then reabsorbed for later use. But some activities hijack the pleasure circuit, either by increasing the amount of dopamine flooding into our systems or by blocking the portals through which the chemical messenger goes back into storage.
The result is a jolt of pleasure so intense that most people will do anything to feel it again.
"Addiction is a super-potent experience," Linden says. And, just like Pavlov's dog, "we learn to associate it with sensory cues," he says, "because these associations allow us to predict how to behave so we can repeat the experience."
When we make a connection between, say, our sweet tooth and a chocolate store located in the Inner Harbor, our brains get rewired. After repeated exposure, structures on our neurons called "dendrites" grow new spines. (The same thing happens when we learn our multiplication tables or memorize a new route to work -- both experiences that humans experience as pleasurable, though to a lesser degree and by a more indirect pathway.)
In the future, every time our car turns onto Pratt Street, we may feel a sudden urge from out of the blue to stop at the chocolatier we know is just down the block.
"If you look at the neurons under a microscope," Linden says, "you will see that the receiving ends of their dendrites have turned into a shaggily bush of spines.
"This is how people develop cravings. If you're an addict, the more times you take a drug, the more spines you'll have on your dendrites and the harder it will be to stay clean, because everything you do will trigger those associations."
There's also another problem. As any chocoholic will confirm, no mouthful will ever deliver a burst of flavor as sublime as the very first taste. In scientific jargon, we've become "habituated."
The gradual draining away of pleasure is the process that Linden is talking about when he describes "liking turning into wanting."
"We imagine that addicts experience more pleasure from their drug of choice than others, and that this motivates their compulsive drug-seeking," he says.
"But the research shows that addicts get less pleasure from their drug than other people. The chemical contact between the neurons gets less efficient over time. It gets worn out. As a result, addicts need higher and higher doses to get as much pleasure as they received the first time they took the drug."
Linden acknowledges that one of his motivations for writing this book was political.
"The Compass of Pleasure" argues that as our laws ignore the biological basis of addiction and instead treat the problem as simply a matter of insufficient willpower that can be resolved by punishment.
"Once we understand how the biology of pleasure works," Linden says, "the only reasonable conclusion that we can make is that addiction is a disease. What we're left with is a compassion model, not a model that says that addicts are losers and should be locked up in jail."
He concludes that if addictions of all types rewire the brain, the eventual solution may lie in devising medicines that can bring about permanent changes on a molecular and cellular level that can undo the damage caused by too many doughnuts, cigarettes or trips to the casino.
There's no question that addicts attempting to kick their habit face an uphill battle -- but Linden isn't letting them off the hook.
"The development of an addiction is not the addict's fault," he says.
"But believing that addiction is a disease does not absolve addicts from responsibility for their own recovery. It's not a free ride."
MW
Baltimore Sun
Johns Hopkins neuroscientist David Linden explains the biology of pleasure
With his new book, he seeks to find out why vices -- and even virtues -- can hold such sway over our lives
By Mary Carole McCauley, The Baltimore Sun
April 14, 2011
Not all addictions live up to their advance press.
In the past decade, it's become common to casually and humorously describe a favorite activity in the parlance of chemical dependency. People speak of being "addicted" to chocolate or high-fat foods, playing video games, buying expensive designer shoes, watching weekly episodes of "American Idol" to sleeping on high-thread-count sheets. But according to "The Compass of Pleasure," a new book by Johns Hopkins neuroscientist David Linden that is being released today by The Viking Press, just two of those pursuits -- eating fatty foods and shopping -- can become genuine addictions for some people. Watching television, playing World of Warcraft and swaddling yourself in Egyptian cotton probably cannot.
Who knew that feeling good could be so complicated?
"Addiction is defined by the changes that certain activities can make in the brain," Linden says.
"Basically, some activities have been shown to short-circuit the medial forebrain pleasure circuit. The process is the same, whether someone is taking crack cocaine or gambling or having risky sex or shopping. These morphological changes bring about a gradual transition from liking to wanting, and the result is compulsive behavior."
The vast majority of people who pursue habit-forming activities will never become compulsive. Our genes play a major role in determining who will become addicted, how badly and to what substance. It also generally takes repeated exposure for a harmful habit to develop.
For example, Linden points out that for even a drug as highly addictive as heroin, two of every three people who inject the narcotic directly into their veins don't become junkies.
In addition, some pursuits that may technically qualify as addictive carry positive benefits for individuals and society that vastly outweigh the potential harm, such as running a marathon, or an extended bout of contemplative prayer.
"Pleasure is our compass, no matter what we do," Linden says.
"But a philosophical question arises from these findings. If we catch a pleasure buzz from our noblest instincts, does that make them less noble?"
Conversely, just because a substance doesn't create a physical dependency doesn't mean it's safe. LSD might not activate the medial forebrain, but someone who drops acid and jumps off the roof because he thinks he can fly is likely to get hurt.
"There's a whole bunch of risk-taking behaviors that aren't addictive," Linden says. "We're motivated by reasons other than seeking pleasure."
Addiction, he says, is just one form of learning. The changes that occur inside the brain when someone studies calculus are nearly identical to the changes that occurs when he smokes crack.
As Linden explains it, when human beings bliss out by watching a sunset, getting a back rub or drinking a glass of red wine, the ventral tegmental area in our brains is releasing a neurotransmitter called dopamine that is getting picked up by a nearby bundle of neurons called the nucleus accumbens.
Under normal circumstances, pleasure flows and ebbs; dopamine gets released and then reabsorbed for later use. But some activities hijack the pleasure circuit, either by increasing the amount of dopamine flooding into our systems or by blocking the portals through which the chemical messenger goes back into storage.
The result is a jolt of pleasure so intense that most people will do anything to feel it again.
"Addiction is a super-potent experience," Linden says. And, just like Pavlov's dog, "we learn to associate it with sensory cues," he says, "because these associations allow us to predict how to behave so we can repeat the experience."
When we make a connection between, say, our sweet tooth and a chocolate store located in the Inner Harbor, our brains get rewired. After repeated exposure, structures on our neurons called "dendrites" grow new spines. (The same thing happens when we learn our multiplication tables or memorize a new route to work -- both experiences that humans experience as pleasurable, though to a lesser degree and by a more indirect pathway.)
In the future, every time our car turns onto Pratt Street, we may feel a sudden urge from out of the blue to stop at the chocolatier we know is just down the block.
"If you look at the neurons under a microscope," Linden says, "you will see that the receiving ends of their dendrites have turned into a shaggily bush of spines.
"This is how people develop cravings. If you're an addict, the more times you take a drug, the more spines you'll have on your dendrites and the harder it will be to stay clean, because everything you do will trigger those associations."
There's also another problem. As any chocoholic will confirm, no mouthful will ever deliver a burst of flavor as sublime as the very first taste. In scientific jargon, we've become "habituated."
The gradual draining away of pleasure is the process that Linden is talking about when he describes "liking turning into wanting."
"We imagine that addicts experience more pleasure from their drug of choice than others, and that this motivates their compulsive drug-seeking," he says.
"But the research shows that addicts get less pleasure from their drug than other people. The chemical contact between the neurons gets less efficient over time. It gets worn out. As a result, addicts need higher and higher doses to get as much pleasure as they received the first time they took the drug."
Linden acknowledges that one of his motivations for writing this book was political.
"The Compass of Pleasure" argues that as our laws ignore the biological basis of addiction and instead treat the problem as simply a matter of insufficient willpower that can be resolved by punishment.
"Once we understand how the biology of pleasure works," Linden says, "the only reasonable conclusion that we can make is that addiction is a disease. What we're left with is a compassion model, not a model that says that addicts are losers and should be locked up in jail."
He concludes that if addictions of all types rewire the brain, the eventual solution may lie in devising medicines that can bring about permanent changes on a molecular and cellular level that can undo the damage caused by too many doughnuts, cigarettes or trips to the casino.
There's no question that addicts attempting to kick their habit face an uphill battle -- but Linden isn't letting them off the hook.
"The development of an addiction is not the addict's fault," he says.
"But believing that addiction is a disease does not absolve addicts from responsibility for their own recovery. It's not a free ride."
Wednesday, April 13, 2011
The Stigma of Chronic Pain
Most of the patients I treat who have chronic pain are distressed by stigma and the ignorance behind it. They are often judged by relatives, friends, doctors, nurses and others as being weak, addicted, defective, "not tough enough," "not motivated." Worst of all is the epithet: "Drug Seeking." Drug Seeking is a judgment impersonating an objective clinical observation. Drug Seeking implies asking for ("seeking") pain medication for non-legitimate purposes, such as getting high, "being a chemical coper," or other reasons not related to pain control. These judgments are almost always made by people who have never experienced unrelenting severe pain. Pain wears you down. No matter how good you are at coping, it pushes you to the edge. If you have other problems such as chronic physical or mental illnesses, it's just that much harder. The more chronic illnesses you have to manage the harder it is to manage any of them very well. When one illness recurs it upsets all the others. I have had patients who stopped taking opioid (narcotic) medications for pain, even though it improved their quality of life and function substantially, because they were stigmatized and criticized by health care providers, families members, and others. They subsequently are condemned to reduced quality of life and reduced personal and employment function in order to not be labeled "drug seeking." The level of knowledge about the management of pain by most clinicians is minimal at best. Chronic pain frequently goes untreated, leading to considerable suffering and disability because of this stigma.
Bottom line: medication that 1) improves overall quality of life, and 2) improved function in the absence of 3) serious side effects should be regarded as life saving, not as a way to escape reality.
MW
Bottom line: medication that 1) improves overall quality of life, and 2) improved function in the absence of 3) serious side effects should be regarded as life saving, not as a way to escape reality.
MW
Saturday, April 9, 2011
Message to Chronic Pain Patients: "Cowboy Up!"
In this recent article in the Washington Post, the growing use of opioid treatment agreements is examined. Although increasing in popularity and pushed strongly by the government (read: DEA) these agreements are at best a mixed blessing. This is all part of a growing sense of unease about using opioids in chronic pain, and a move to further restrict access to them. These agreements may do more to protect the prescriber from liability than to protect patients. What is clear to physicians, however, is that there is no liability from refusing to prescribe opioids even if it leads to serious consequences including disability and suicide because patients are held responsible for them. On the other hand, doctors feels the hot breath of the DEA and state medical boards and the threat of malpractice suites very acutely. As with all medications, opioids carry a risk and it is important to minimize it, but even very reasonable risk in the context of substantial benefit is fraught with danger for the physician. It seems that there are plenty of doctors around who will testify against any doctor prescribing opioids for chronic pain. As I have said before, the vacuum created by the lack of good evidence is filled with strong opinion, often passionately held, and usually by those who take a highly moralistic approach to the issue. The end result is not a reduced risk to patients but increasing restriction on access to appropriate opioid medication for chronic pain. This past year, an opioid addicted nurse at a Minneapolis hospital stole a patient's medications that were to be used for his surgery, and told him he was going to have to "cowboy up." He had surgery without analgesia. That pretty well sums up the message to pain patients from regulatory agencies and doctors antagonistic to opioids. This is not going to change until patients and families put the heat on legislatures and Congress to fund more research in this area, and to back off the persecution of doctors who are trying their best to balance risk and benefit in this most terrible affliction.
MW
Some doctors require patients to sign contracts get opioid painkillers
By Michelle Andrews, Monday, April , 4:38 PM
Chronic pain — the kind that lasts for months or recurs regularly — afflicts more than a quarter of adult Americans. Treating pain can be extremely challenging, however, in part because it can’t be measured with instruments. It’s in the eye — or neck or joint — of the beholder.
Doctors often prescribe powerful painkillers called opioids — natural or synthetic versions of opium. Sometimes the prescription is for short-term, acute pain: If you’ve ever had a root canal or surgery or thrown out your back, you may have received a prescription for Percocet or Vicodin, both of which are opioids that also contain acetaminophen.
For people with long-term, persistent pain — often from musculoskeletal injuries or nerve damage — opioids may be the best option to manage their pain and enable them to function day after day.
But there’s a hitch: Though highly effective, these drugs are dangerous and addictive. The chief danger is that they can cause respiratory depression: If too much is taken, breathing slows and may eventually stop. And because they cause euphoria, opioids are popular targets for misuse and abuse. In 2007, 11,499 people in the United States died from opioid overdoses, according to the Centers for Disease Control and Prevention. That was more than the number of overdose deaths for heroin and cocaine combined. To help monitor use of the drugs, some doctors ask patients to sign “pain contracts” or “opioid treatment agreements” that spell out the rules patients must follow to take these drugs safely. The contracts aim to discourage people from taking too much medication, mixing medications, or sharing or selling them, among other things.
The agreements may require patients to submit to blood or urine drug tests, fill their prescriptions at a single pharmacy or refuse to accept pain medication from any other doctor. If patients don’t follow the rules, the agreements often state that doctors may drop them from their practice.
Some patient advocates and policy experts say that rather than ensuring safety, the agreements invade patients’ privacy and damage the trust that’s essential to the doctor-patient relationship.
Joan Crowley started taking an opioid in 2003 to treat recurring migraines and an arthritis-like autoimmune disorder that caused her joints to swell. The drug kept her pain under control and allowed her to continue her work as an accountant in the Pittsburgh area.
A few years ago, her primary-care provider asked her to sign a treatment agreement for the opioid and for Xanax, an anti-anxiety drug she also took regularly. Every three months she visited the doctor so he could evaluate her condition and write her a new round of prescriptions. Sometimes he did a urine test as well.
All went smoothly until this past winter. Crowley, 51, went to the emergency room with what she thought was a heart attack but turned out to be anxiety. While there, she says, she was given an anti-anxiety drug and other medications. The next day she had her regular appointment with her doctor, who gave her prescriptions for her regular drugs and took a urine sample. A week later, she says, she got a telephone call from him, saying that an opioid she wasn’t supposed to be taking had turned up in her urine sample. The doctor gave her 60 days to find a new physician — even after she told him about her ER visit.
Crowley acknowledges that her relationship with the doctor had been strained before that. Still, she was stunned. “This is someone I’d been a patient of for 11 years,” she says. “There was a level of trust there.”
Because of a few high-profile prosecutions of doctors for running “pill mills,” some experts say, doctors increasingly use pain contracts to protect themselves.
The subjective nature of pain makes doctors afraid they’ll be scammed by unscrupulous patients, says Myra Christopher, chief executive of the Center for Practical Bioethics in Kansas City, Mo., who co-authored a recent article critical of pain contracts. “Providers’ primary concern ought to be the management of pain and suffering,” she says. “This shifts the locus of concern to the providers’ protection.”
Others disagree. They say treatment agreements can function as an educational tool and a treatment road map. “It provides a framework to talk about the issues that come up in a treatment plan,” says S. Hughes Melton, a family physician in rural Lebanon, Va., where substance abuse, including addiction to pain medication, is a serious problem.
After working in the mining industry for 22 years, Jeffery Boyd, 50, developed continual pain in his back and legs. Working with Melton, he manages his pain with an opioid and another drug. To Boyd, signing a treatment agreement and being closely monitored by Melton are secondary concerns: Mostly he’s just glad to have his pain under control. “The pain won’t ever go away,” he says, “but [Melton] got me to where I can work at my job and do things.”
That attitude is probably shared by many people with chronic pain, say experts. “Most patients who come in, they just want relief,” says Will Rowe, chief executive of the American Pain Foundation, a consumer advocacy group. “They don’t want to hear about the public-health problem of the misuse of opioids.”
This column is produced through a collaboration between The Post and Kaiser Health News. KHN, an editorially independent news service, is a program of the Kaiser Family Foundation, a nonpartisan health-care-policy organization that is not affiliated with Kaiser Permanente. E-mail questions@kaiserhealthnews.org.
MW
Some doctors require patients to sign contracts get opioid painkillers
By Michelle Andrews, Monday, April , 4:38 PM
Chronic pain — the kind that lasts for months or recurs regularly — afflicts more than a quarter of adult Americans. Treating pain can be extremely challenging, however, in part because it can’t be measured with instruments. It’s in the eye — or neck or joint — of the beholder.
Doctors often prescribe powerful painkillers called opioids — natural or synthetic versions of opium. Sometimes the prescription is for short-term, acute pain: If you’ve ever had a root canal or surgery or thrown out your back, you may have received a prescription for Percocet or Vicodin, both of which are opioids that also contain acetaminophen.
For people with long-term, persistent pain — often from musculoskeletal injuries or nerve damage — opioids may be the best option to manage their pain and enable them to function day after day.
But there’s a hitch: Though highly effective, these drugs are dangerous and addictive. The chief danger is that they can cause respiratory depression: If too much is taken, breathing slows and may eventually stop. And because they cause euphoria, opioids are popular targets for misuse and abuse. In 2007, 11,499 people in the United States died from opioid overdoses, according to the Centers for Disease Control and Prevention. That was more than the number of overdose deaths for heroin and cocaine combined. To help monitor use of the drugs, some doctors ask patients to sign “pain contracts” or “opioid treatment agreements” that spell out the rules patients must follow to take these drugs safely. The contracts aim to discourage people from taking too much medication, mixing medications, or sharing or selling them, among other things.
The agreements may require patients to submit to blood or urine drug tests, fill their prescriptions at a single pharmacy or refuse to accept pain medication from any other doctor. If patients don’t follow the rules, the agreements often state that doctors may drop them from their practice.
Some patient advocates and policy experts say that rather than ensuring safety, the agreements invade patients’ privacy and damage the trust that’s essential to the doctor-patient relationship.
Joan Crowley started taking an opioid in 2003 to treat recurring migraines and an arthritis-like autoimmune disorder that caused her joints to swell. The drug kept her pain under control and allowed her to continue her work as an accountant in the Pittsburgh area.
A few years ago, her primary-care provider asked her to sign a treatment agreement for the opioid and for Xanax, an anti-anxiety drug she also took regularly. Every three months she visited the doctor so he could evaluate her condition and write her a new round of prescriptions. Sometimes he did a urine test as well.
All went smoothly until this past winter. Crowley, 51, went to the emergency room with what she thought was a heart attack but turned out to be anxiety. While there, she says, she was given an anti-anxiety drug and other medications. The next day she had her regular appointment with her doctor, who gave her prescriptions for her regular drugs and took a urine sample. A week later, she says, she got a telephone call from him, saying that an opioid she wasn’t supposed to be taking had turned up in her urine sample. The doctor gave her 60 days to find a new physician — even after she told him about her ER visit.
Crowley acknowledges that her relationship with the doctor had been strained before that. Still, she was stunned. “This is someone I’d been a patient of for 11 years,” she says. “There was a level of trust there.”
Because of a few high-profile prosecutions of doctors for running “pill mills,” some experts say, doctors increasingly use pain contracts to protect themselves.
The subjective nature of pain makes doctors afraid they’ll be scammed by unscrupulous patients, says Myra Christopher, chief executive of the Center for Practical Bioethics in Kansas City, Mo., who co-authored a recent article critical of pain contracts. “Providers’ primary concern ought to be the management of pain and suffering,” she says. “This shifts the locus of concern to the providers’ protection.”
Others disagree. They say treatment agreements can function as an educational tool and a treatment road map. “It provides a framework to talk about the issues that come up in a treatment plan,” says S. Hughes Melton, a family physician in rural Lebanon, Va., where substance abuse, including addiction to pain medication, is a serious problem.
After working in the mining industry for 22 years, Jeffery Boyd, 50, developed continual pain in his back and legs. Working with Melton, he manages his pain with an opioid and another drug. To Boyd, signing a treatment agreement and being closely monitored by Melton are secondary concerns: Mostly he’s just glad to have his pain under control. “The pain won’t ever go away,” he says, “but [Melton] got me to where I can work at my job and do things.”
That attitude is probably shared by many people with chronic pain, say experts. “Most patients who come in, they just want relief,” says Will Rowe, chief executive of the American Pain Foundation, a consumer advocacy group. “They don’t want to hear about the public-health problem of the misuse of opioids.”
This column is produced through a collaboration between The Post and Kaiser Health News. KHN, an editorially independent news service, is a program of the Kaiser Family Foundation, a nonpartisan health-care-policy organization that is not affiliated with Kaiser Permanente. E-mail questions@kaiserhealthnews.org.
Thursday, March 31, 2011
New Drugs Boost Response Rates in Hepatitis C
Good news for those who have chronic hepatitis C, which affects people with addictions much more frequently than others. Two new drugs have been shown to substantially improve sustained remission rates in the Genotype I type of the virus, which is the most common type of infection in the US. Importantly, although the response rate was lower in African Americans (due to genetic factors limiting the drug effectiveness), these drugs improved response rates to respectable levels. The new medications are awaiting approval by the FDA and may be on the market as early as last 2011.
MW
New drug boosts hepatitis C treatments
Experimental medication passes key test on road to FDA approval for treating virus By Nathan Seppa
Science News
Web edition : 10:35 am
Adding an experimental drug to standard treatment more than doubles the likelihood of knocking out hepatitis C in patients with the chronic liver infection, two studies in the March 31 New England Journal of Medicine show.
The new drug, boceprevir, and a similar drug called telaprevir (SN: 5/23/09, p. 12) have now shown the ability to wipe out the virus in many patients. Both drugs are currently under review by the Food and Drug Administration, and scientists feel that both are destined for approval.
“This is the first time I can remember being so optimistic about this really difficult virus,” says Donald Jensen, a hepatologist at the University of Chicago School of Medicine who wasn’t involved in the new studies. Hepatitis C can lead to liver cirrhosis and cancer.
Both new boceprevir trials started with hundreds of hepatitis C patients receiving a four-week course of the current standard medication, a one-two punch of drugs called peginterferon alfa-2b and ribavirin. The patients were then randomly assigned to get boceprevir or a placebo added to this regimen, without knowing which they were getting.
After receiving treatment for up to 44 weeks, those getting boceprevir were two to three times more likely to knock the virus down to undetectable levels in the blood as were those getting only the standard dual-drug therapy, researchers report.
The two trial groups weren’t identical: One recruited previously treated hepatitis C patients, while the other enlisted only patients who hadn’t yet been treated. But both studies showed viral clearance rates of nearly two-thirds among those getting the triple therapy, compared with only 21 to 38 percent success among those getting the standard regimen.
A patient who clears the virus is often cured, says Fred Poordad, a hepatologist at Cedars-Sinai Medical Center in Los Angeles, who coauthored both studies. He cites 10 years of follow-up data from people who had cleared the virus after getting the standard peginterferon/ribavirin treatment. If the virus doesn’t reappear within six months after treatment, he says, close to 100 percent of them remain free of virus for good.
But 25 to 30 percent of those receiving standard treatment typically experience such a relapse shortly after treatment. With boceprevir added to the mix, that figure can be expected to fall below 10 percent, Poordad says.
The results thus indicate that 60 to 70 percent of patients getting the triple therapy “are now cured,” says Bruce Bacon, a hepatologist at Saint Louis University School of Medicine who coauthored both of the new studies.
The treatment does carry side effects. In both trials, nearly half of patients getting boceprevir developed anemia, compared with 20 to 29 percent of those on the standard dual treatment. Anemia is treatable, Bacon says. Nearly all patients in both trials reported some other side effects — including fatigue, headache and nausea — while taking the drug regimen. Bacon acknowledges these adverse effects, but adds that most hepatitis C patients “are willing to tough it out.”
Black patients didn’t benefit as much from the treatment as did other racial groups because some blacks carry a genetic variant that limits the effect of the drugs, Jensen says. Even so, roughly half of blacks getting the triple treatment saw their virus fall below detectable levels, a substantially better rate than those on dual therapy.
Merck makes boceprevir and sponsored these two trials. Vertex Pharmaceuticals makes telaprevir. Bacon notes that these studies now show that the effectiveness of boceprevir and telaprevir are similar. That’s not surprising since both drugs inhibit protease enzymes. While protease enzymes play vital roles in the body, thwarting specific proteases can stall virus replication.
The drugs work only on genotype 1 hepatitis C, but that form accounts for about three-fourths of all hepatitis C in the United States.
MW
New drug boosts hepatitis C treatments
Experimental medication passes key test on road to FDA approval for treating virus By Nathan Seppa
Science News
Web edition : 10:35 am
Adding an experimental drug to standard treatment more than doubles the likelihood of knocking out hepatitis C in patients with the chronic liver infection, two studies in the March 31 New England Journal of Medicine show.
The new drug, boceprevir, and a similar drug called telaprevir (SN: 5/23/09, p. 12) have now shown the ability to wipe out the virus in many patients. Both drugs are currently under review by the Food and Drug Administration, and scientists feel that both are destined for approval.
“This is the first time I can remember being so optimistic about this really difficult virus,” says Donald Jensen, a hepatologist at the University of Chicago School of Medicine who wasn’t involved in the new studies. Hepatitis C can lead to liver cirrhosis and cancer.
Both new boceprevir trials started with hundreds of hepatitis C patients receiving a four-week course of the current standard medication, a one-two punch of drugs called peginterferon alfa-2b and ribavirin. The patients were then randomly assigned to get boceprevir or a placebo added to this regimen, without knowing which they were getting.
After receiving treatment for up to 44 weeks, those getting boceprevir were two to three times more likely to knock the virus down to undetectable levels in the blood as were those getting only the standard dual-drug therapy, researchers report.
The two trial groups weren’t identical: One recruited previously treated hepatitis C patients, while the other enlisted only patients who hadn’t yet been treated. But both studies showed viral clearance rates of nearly two-thirds among those getting the triple therapy, compared with only 21 to 38 percent success among those getting the standard regimen.
A patient who clears the virus is often cured, says Fred Poordad, a hepatologist at Cedars-Sinai Medical Center in Los Angeles, who coauthored both studies. He cites 10 years of follow-up data from people who had cleared the virus after getting the standard peginterferon/ribavirin treatment. If the virus doesn’t reappear within six months after treatment, he says, close to 100 percent of them remain free of virus for good.
But 25 to 30 percent of those receiving standard treatment typically experience such a relapse shortly after treatment. With boceprevir added to the mix, that figure can be expected to fall below 10 percent, Poordad says.
The results thus indicate that 60 to 70 percent of patients getting the triple therapy “are now cured,” says Bruce Bacon, a hepatologist at Saint Louis University School of Medicine who coauthored both of the new studies.
The treatment does carry side effects. In both trials, nearly half of patients getting boceprevir developed anemia, compared with 20 to 29 percent of those on the standard dual treatment. Anemia is treatable, Bacon says. Nearly all patients in both trials reported some other side effects — including fatigue, headache and nausea — while taking the drug regimen. Bacon acknowledges these adverse effects, but adds that most hepatitis C patients “are willing to tough it out.”
Black patients didn’t benefit as much from the treatment as did other racial groups because some blacks carry a genetic variant that limits the effect of the drugs, Jensen says. Even so, roughly half of blacks getting the triple treatment saw their virus fall below detectable levels, a substantially better rate than those on dual therapy.
Merck makes boceprevir and sponsored these two trials. Vertex Pharmaceuticals makes telaprevir. Bacon notes that these studies now show that the effectiveness of boceprevir and telaprevir are similar. That’s not surprising since both drugs inhibit protease enzymes. While protease enzymes play vital roles in the body, thwarting specific proteases can stall virus replication.
The drugs work only on genotype 1 hepatitis C, but that form accounts for about three-fourths of all hepatitis C in the United States.
Tuesday, March 29, 2011
How Cocaine Changes the Brain
This new research identifies how cocaine changes the configuration of receptors and function in the reward areas of the brain. It adds to the evidence that an increase in glutamate is a key feature of addiction. Some of the medications currently used for alcohol dependence, such as topiramate, baclofen and acamprosate, may work by helping to restore the balance between glutamate and GABA.
MW
Cocaine inverts rules for synaptic plasticity of glutamate transmission in the ventral tegmental area
Manuel Mameli, Camilla Bellone, Matthew T C Brown & Christian Lüscher
Nature Neuroscience (2011) 14, 414-416
The manner in which drug-evoked synaptic plasticity affects reward circuits remains largely elusive. We found that cocaine reduced NMDA receptor excitatory postsynaptic currents and inserted GluA2–lacking AMPA receptors in dopamine neurons of mice. Consequently, a stimulation protocol pairing glutamate release with hyperpolarizing current injections further strengthened synapses after cocaine treatment. Our data suggest that early cocaine-evoked plasticity in the ventral tegmental area inverts the rules for activity-dependent plasticity, eventually leading to addictive behavior.
MW
Cocaine inverts rules for synaptic plasticity of glutamate transmission in the ventral tegmental area
Manuel Mameli, Camilla Bellone, Matthew T C Brown & Christian Lüscher
Nature Neuroscience (2011) 14, 414-416
The manner in which drug-evoked synaptic plasticity affects reward circuits remains largely elusive. We found that cocaine reduced NMDA receptor excitatory postsynaptic currents and inserted GluA2–lacking AMPA receptors in dopamine neurons of mice. Consequently, a stimulation protocol pairing glutamate release with hyperpolarizing current injections further strengthened synapses after cocaine treatment. Our data suggest that early cocaine-evoked plasticity in the ventral tegmental area inverts the rules for activity-dependent plasticity, eventually leading to addictive behavior.
Sunday, March 27, 2011
Treating Pain Is a Real Pain
Our current tools for treating chronic severe pain are inadequate at best. Opioids such as morphine or methadone reduce chronic pain on average about 30%, with a range of perhaps 0-50%. And of course they come with multiple liabilities, such as constipation, sweating, nausea and physiological tolerance which means that symptoms occur if the drug is suddenly stopped. Although unproven there is concern that chronic use of these medications could actually increase pain sensitivity. Other methods such as cognitive behavioral therapy, moderate exercise, physical therapy, injections, surgery, neurostimulators, biofeedback, etc., have a modest impact if any. We desperately need new tools. This article describes new research on a compound that may reduce pain without the disadvantages of opioids. Cannabinoid receptors, by the way, are those that responde to drugs like marijuana and hashish. There are more of these receptors in peripheral tissues than the brain. It is possible that the effect of cannabis on pain are due to their effects on these peripheral receptors.
MW
Anandamide suppresses pain initiation through a peripheral endocannabinoid mechanism
Jason R Clapper, Guillermo Moreno-Sanz, Roberto Russo, Ana Guijarro, Federica Vacondio, Andrea Duranti, Andrea Tontini, Silvano Sanchini, Natale R Sciolino, Jessica M Spradley, Andrea G Hohmann, Antonio Calignano, Marco Mor, Giorgio Tarzia & Daniele Piomelli
Nature Neuroscience 13, 1265–1270 (2010) doi:10.1038/nn.2632
Peripheral cannabinoid receptors exert a powerful inhibitory control over pain initiation, but the endocannabinoid signal that normally engages this intrinsic analgesic mechanism is unknown. To address this question, we developed a peripherally restricted inhibitor (URB937) of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of the endocannabinoid anandamide. URB937 suppressed FAAH activity and increased anandamide levels outside the rodent CNS. Despite its inability to access brain and spinal cord, URB937 attenuated behavioral responses indicative of persistent pain in rodent models of peripheral nerve injury and inflammation and prevented noxious stimulus–evoked neuronal activation in spinal cord regions implicated in nociceptive processing. CB1 cannabinoid receptor blockade prevented these effects. These results suggest that anandamide-mediated signaling at peripheral CB1 receptors controls the access of pain-related inputs to the CNS. Brain-impenetrant FAAH inhibitors, which strengthen this gating mechanism, might offer a new approach to pain therapy.
MW
Anandamide suppresses pain initiation through a peripheral endocannabinoid mechanism
Jason R Clapper, Guillermo Moreno-Sanz, Roberto Russo, Ana Guijarro, Federica Vacondio, Andrea Duranti, Andrea Tontini, Silvano Sanchini, Natale R Sciolino, Jessica M Spradley, Andrea G Hohmann, Antonio Calignano, Marco Mor, Giorgio Tarzia & Daniele Piomelli
Nature Neuroscience 13, 1265–1270 (2010) doi:10.1038/nn.2632
Peripheral cannabinoid receptors exert a powerful inhibitory control over pain initiation, but the endocannabinoid signal that normally engages this intrinsic analgesic mechanism is unknown. To address this question, we developed a peripherally restricted inhibitor (URB937) of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of the endocannabinoid anandamide. URB937 suppressed FAAH activity and increased anandamide levels outside the rodent CNS. Despite its inability to access brain and spinal cord, URB937 attenuated behavioral responses indicative of persistent pain in rodent models of peripheral nerve injury and inflammation and prevented noxious stimulus–evoked neuronal activation in spinal cord regions implicated in nociceptive processing. CB1 cannabinoid receptor blockade prevented these effects. These results suggest that anandamide-mediated signaling at peripheral CB1 receptors controls the access of pain-related inputs to the CNS. Brain-impenetrant FAAH inhibitors, which strengthen this gating mechanism, might offer a new approach to pain therapy.
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