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Posted by Dr. Jeff and Dr. Tanya on February 03, 2009 at 07:31 AM in Addictions: Drug Abuse | Permalink | Comments (0)
A number of our Nation's best monitoring mechanisms have detected an alarming increase in the popularity of MDMA (3,4-methylenedioxymethamphetamine), particularly among young Americans. Unfortunately, myths abound about both the acute effects and long-term consequences of this drug, also known as "Ecstasy," with many young people believing that MDMA is safe, offering nothing but a pleasant high for the $25 cost of a single tablet. But MDMA is not new to the scientific community, with many laboratories beginning their investigations of this drug in the mid 1980s, and the picture emerging from their efforts paints a much different image of this drug, one that is far from benign.
This report, Ecstasy: What We Know and Don't Know About MDMA, represents a scientific review of what research has discovered about how this drug works in the brain and what requires further study to fully understand the consequences of using this illicit substance. This report discusses what scientists know and don't know about MDMA's acute effects on the brain and behavior from laboratory studies in both animals and humans. The report also reviews the long-term effects on the brain, again in both laboratory animals and humans, as well as long-term behavioral consequences detected in chronic MDMA users.
MDMA, a relatively simple chemical belonging to the amphetamine family of compounds, has properties of both stimulants and hallucinogens. While MDMA does not cause true hallucinations, many people have reported distorted time and perception while under the influence of this drug. The vast majority of people take MDMA orally, and its effects last approximately four to six hours. Many users will "bump" the drug, taking a second dose when the effects of the initial dose begin to fade. The typical dose is between one and two tablets, with each containing approximately 60-120 milligrams of MDMA. However, tablets of what users call Ecstasy often contain not only MDMA but a number of other drugs, including methamphetamine, caffeine, dextromethorphan, ephedrine, and cocaine.
One of the more alarming facts about MDMA is that despite its known detrimental effects, there are increasing numbers of students and young adults who continue to use the drug. Results from the 2000 Monitoring the Future survey indicate that MDMA use increased among students in the 12th, 10th, and 8th grades. African Americans show considerably lower rates of MDMA use than do either whites or Hispanics. The recent CEWG data showed a large increase in use among Hispanics that may represent an important change.
MDMA works in the brain by increasing the activity levels of at least three neurotransmitters: serotonin, dopamine, and norepinepherine. Much like other amphetamines, MDMA causes these neurotransmitters to be released from their storage sites in neurons, increasing brain activity. Compared to the potent stimulant methamphetamine, MDMA triggers a larger increase in serotonin and a smaller increase in dopamine. Serotonin is a major neurotransmitter involved in regulating mood, sleep, pain, emotion, and appetite, as well as other behaviors. By releasing large amounts of serotonin, and also interfering with its synthesis, MDMA leads to a significant depletion of this important neurotransmitter. As a result, it takes the human brain a significant amount of time to rebuild the store of serotonin needed to perform important physiological and psychological functions.
One hypothesis to explain the long-lasting neurotoxicity of MDMA on serotonergic systems is that MDMA induces both oxidative and metabolic stress in serotonin neurons that, in turn, adversely affect the ability of these neurons to produce serotonin. Support for this hypothesis comes from a variety of studies, including those showing that MDMA perturbs the activity of various antioxidant enzymes; artificially boosting the levels of these enzymes reduces MDMA's effects on serotonin and dopamine neurons. Also, stress appears to increase the oxidative damage caused by MDMA.
It has been difficult to study the effects of MDMA in humans under controlled conditions, and virtually impossible until recently to conduct simultaneous neurochemical studies. However, several groups of researchers have chosen to study the behavioral pharmacology of MDMA in various animal species, showing that MDMA and related compounds produce a unique behavioral profile in rodents. Studies in non-human primates suggests that acute doses of MDMA may have subtle effects on higher cognitive functions, including memory and learning. Other experiments in laboratory animals suggest that MDMA is a drug that humans are likely to abuse, and that humans may develop tolerance to MDMA's reinforcing effects. Limited studies in humans have shown that MDMA negatively impacts short-term performance on a variety of measures of cognitive ability.
Controlled studies in humans have shown that MDMA has potent effects on the cardiovascular system and on the body's ability to regulate its internal temperature. Of great concern is MDMA's adverse effect on the pumping efficiency of the heart - in the presence of MDMA, increased physical activity increases heart rate significantly, but the heart does not respond in its normal manner, which is to increase the efficiency with which it pumps blood. Since MDMA use is often associated with sustained, strenuous activity, such as dancing, MDMA's effects on the heart could increase the risk of heart damage or other cardiovascular complications in susceptible individuals.
Pharmacokinectic studies have shown that MDMA is rapidly absorbed into the human blood stream, but once in the body the metabolites of MDMA inhibit MDMA metabolism. As a result, subsequent doses of the drug produce unexpectedly high blood levels, which could worsen the cardiovascular and other adverse effects of this drug without increasing its "pleasurable" effects, which tend to peak about two hours after taking an initial dose. MDMA interferes with the metabolism of other drugs, including some of the adulterants in MDMA tablets.
Acute doses of MDMA produce marked changes in both dopamine and serotonin systems within the brain. Though the changes in dopaminergic neurons appear transient, the data suggest that the changes in the serotonergic system are longer-lasting. In addition, examinations of more global brain function have shown that the effects of acute doses of MDMA extend to regions of the brain that are thought to be involved in higher thought processes. These findings have raised concern about possible long-term effects on both infrequent and regular users of MDMA.
Several groups have shown that exposure to MDMA rapidly and persistently destroys a key marker of serotonergic function in regions known to have a high density of serotonin neurons, including the striatum and cortex. More detailed examination of this structural damage shows that MDMA appears to prune, or reduce in number, serotonin axons and axon terminals. Eighteen months after a short course of MDMA, investigators found that some brain regions had substantial loss of serotonin axon terminals, while a few others had more serotonin axon terminals. This pattern is a hallmark of axon pruning, since nerve cells will often grow replacement terminals upstream of the damaged terminals. These results, then, are evidence not only of MDMA's neurotoxicity, but of the brain attempting to rewire the serotonin system after damage.
Since younger brains may have an increased susceptibility to the neurotoxic effects of MDMA, it may be that the youngest, fastest developing brains - those of a developing fetus - could be particularly vulnerable to the effects of this apparent serotonin neurotoxin. Since most MDMA users are young and in their reproductive years, it is possible that some female users may take MDMA when they are pregnant, either inadvertently or intentionally, because of the misperception that it is a safe drug. Studies in animals have shown that MDMA has little effect on the physical development of the young brain. Behavioral and cognitive studies in laboratory animals, however, have identified significant adverse cognitive effects from pre and neonatal exposure to MDMA. This effect was not due to serotonergic neurotoxicity; the mechanisms underlying the development of these cognitive deficits are not known yet. Though the rodent experiments have predictive value, it is not known whether human fetuses exposed to MDMA when their mothers abuse the drug will develop persistent and learning memory deficits.
Because MDMA produces long-term deficits in serotonin function, and because serotonin function has been implicated in the etiology of many psychiatric disorders including depression and anxiety, investigators have suspected that MDMA users may experience more psychopathology than non-users. Indeed, a number of investigators have found that heavy MDMA users experience a constellation of psychiatric changes, scoring significantly higher on measures of obsessive traits, anxiety, paranoid thoughts, and disturbed sleep, among others. One study, aimed at developing reliable measures of diagnosing substance abuse disorders, found that 43 percent of MDMA users met DSM-IV criteria for dependence and 34 percent met the criteria for abuse of MDMA.
There is a large and growing body of evidence from a variety of studies with humans that MDMA use can have long-lasting effects on memory. None of these studies are perfect, as they all have methodological concerns such as concurrent use of other drugs (it is apparently impossible to find but a few MDMA users who do not use other illicit substances, particularly marijuana). In addition, results vary with the assessment used. Nonetheless, the general finding that emerges across all of the studies is that MDMA does impact memory abilities in ways that could adversely affect normal functioning on every day tasks. Moreover, the relationship between memory problems and MDMA use appears to have a dose-dependent relationship, that is, the more MDMA used, the greater the deficit.
Given that numerous studies have shown that the serotonin deficits caused by MDMA are persistent, lasting at least seven years in one study of nonhuman primates, it is important to determine if the psychological and memory deficits associated with even moderate use of MDMA recover after some period of time. This is a particularly important issue with MDMA because of the relatively young age of the majority of people who abuse this drug. So far, the majority of studies have focused on MDMA users who have been abstinent for a period of a few weeks to a few months - longer-term studies have been planned or are underway - and these have shown that the adverse psychiatric and cognitive changes associated with MDMA use are persistent.
In attempting to answer the question of whether MDMA causes permanent damage to human memory abilities, there is no one study that provides a resounding, definitive yes. To be sure, no study provides any evidence that MDMA is a beneficial drug or even that it is safe when taken in moderation. In fact taking MDMA at any dose carries with it the risk of inducing physiological, psychological, and cognitive damage in vulnerable users. Clearly, there is still room to debate the exact nature of the deficits produced by MDMA use. Nevertheless, based on the results from the overwhelming majority of studies conducted so far, the data show that MDMA can be harmful to human health.
As much as the data collected so far largely supports the proposition that MDMA damages the serotonin system in the brain and produces long-lasting behavioral deficits, researchers agree that methodological issues, such as limited sample size and difficulties controlling for the possible influence of other illicit substances, have made it difficult to move beyond generalities and unequivocally prove a cause and effect relationship between MDMA use and specific cognitive or psychological damage in humans.
All of the studies reviewed in this report have relied on self-referred MDMA users, recruited through targeted sampling techniques by advertising for volunteers or through word-of-mouth. This introduces an unknown bias into each study since it is possible that such self-referrers are not representative of MDMA users as a whole. There is also the problem of verifying that what users report as Ecstasy is, in fact, solely MDMA. In addition, it is impossible to verify self-reports of past drug use beyond a certain period of time, making it difficult at best to accurately control for prior drug use.
Since there seem to be few, if any, young people who use MDMA without also abusing other drugs, this will continue to be a confounding factor in future studies. Some investigators have tried to accommodate this problem by using a control group comprising individuals who have never used MDMA but who otherwise have closely matched histories of using other drugs of abuse. This type of control has not been used universally, however, and even when it is, it may be difficult to closely match users and controls for prior drug use, as well as on other demographic details such as educational level and age.
Self-reporting also means that it is not possible to determine with complete confidence or accuracy how much a person has consumed, either on a particular occasion or over a lifetime of use. This uncertainty arises for two reasons: MDMA content is not constant across all tablets, and user memory of how much and how often a person took MDMA over many years is far from reliable.
Ideally, researchers would like to be able to study MDMA's effects in drug-naïve humans, and indeed, a limited number of groups in Europe have received approval from the appropriate governmental regulatory agencies and institutional review boards to conduct what would essentially be Phase I safety trials with MDMA in a limited number of humans. However, there is little likelihood of studying the effects of MDMA on large numbers of drug-naïve volunteers. An alternative might be to conduct longitudinal, controlled prospective studies, in which current MDMA users and controls of non-MDMA users are followed for many years to observe changes from some defined baseline.
Though the data presented at this conference and in the literature support the hypothesis that MDMA produces acute behavioral and physiological effects, there is still more to be determined about factors that precipitate severe acute toxicity. For example, are there predisposing genetic factors that increase the risk for acute toxicity? Is overall health status important? Which organs and systems are the primary targets of MDMA toxicity? Are interactions with other drugs important? Does MDMA use lead to tolerance, withdrawal, and craving?
Because MDMA is not the only drug taken by young adults, there is a need for more characterization of interactions between these substances and a determination of how those drug interactions may influence acute toxicity. Is the practice of "bumping" or taking sequential doses of MDMA particularly dangerous? How do individual genetic factors influence MDMA metabolism and drug interactions?
One critical piece of missing data is the incidence of acute toxicity among MDMA users. Assembling this database will require improved emergency room reporting of MDMA-associated incidents. In addition, data do not yet exist on the number of people seeking treatment for MDMA-related dependence and behavioral or psychological problems.
One of the key concerns raised at the meeting was the lack of longitudinal studies designed to follow MDMA users, both as they continue to use the drug and after they have stopped using it. Such studies may provide important insight into how age and length of use affect MDMA's acute and long-term neurochemical toxicity. In addition, such studies would allow researchers to determine if deficits appear later in life, long after use stops, or if adverse effects diminish over time. Such studies, if designed with regular assessment intervals, might also allow researchers to develop better measures of MDMA toxicity, and to more accurately determine how much drug is used and in what circumstances.
If conducted with large enough groups of MDMA users and control subjects, both drug naïve and matched for poly-drug use, longitudinal studies could also help identify risk and protective factors for drug use and the deficits that result from continuing exposure to MDMA. The identification of significant risk and protective factors would greatly aid the development of efficacious prevention and rehabilitation approaches. Data from longitudinal studies would also help establish associations between MDMA use and behavioral impairments that researchers have observed in the majority of studies.
Longitudinal designs may enable researchers to determine how long such impairments last, whether they are progressive, and if deficits become more evident as MDMA users move into middle and late adulthood or experience other age-related neurologic disorders. Questions about the reversibility of impairments, a concern given the data seen in animal studies and even in some human studies, could also be addressed by such designs. Longitudinal studies should also provide data on critical patterns of MDMA use that may be more or less likely to cause impairments, and can help to determine whether simultaneous abuse of other drugs plays a role in causing behavioral and cognitive damage.
Along with such studies, researchers need better tools to assess neurotoxicity in human MDMA users and to measure changes of neuronal integrity and possible recovery over time. With such tools, investigators may also be able to address important mechanistic questions, such as how damage to the serotonin system leads to behavioral and cognitive changes, how the brain responds to and compensates for serotonergic damage, and why the dopaminergic system seems to escape lasting damage from MDMA. Such studies might then lead to the development and validation of methods for promoting recovery from MDMA-induced neurotoxicity.
There is also a need for more studies looking at the long-term effects of poly-drug abuse. Such studies will require new analytical tools for detecting multiple drugs of abuse simultaneously in biological samples and for more accurately assessing drug use histories, including the combination and sequencing of drugs used.
There are little data available on whether addiction, dependence or tolerance develops with continued use of MDMA. Though the data from animal studies support this possibility, more studies are needed in humans to determine the degree of abuse liability for this drug and to help develop treatments specific for reducing MDMA addiction. Along the same lines, researchers at this meeting stressed again that there are little data on numbers of drug treatment patients who have used MDMA or who have sought treatment because of MDMA abuse.
Another scientific gap idenitfied at the scientific conference concerns the development of methods for tracking so-called hidden populations of MDMA users; that is, those who don't go to dance clubs or raves, where the majority of volunteer recruiting occurs. At the same time, researchers also stressed the need to better understand the youth party culture that seems to actively promote MDMA use through the use of in-house drug dealers and marketing messages delivered through music and by pop icons.
There is a need to foster interdisciplinary research and dialogue that links epidemiological, ethnographic, clinical and laboratory studies. As this report shows, there is much overlap between these separate fields, and undoubtedly, this area of investigation could benefit from better coordination between disciplines. There is also a need to link local, regional, national, and international supply-side intelligence with demand-side epidemiological and ethnographic research.
Prevention efforts cannot be universal but must be targeted at different groups that use MDMA, particularly since MDMA appears to be a drug whose use is sensitive to and intimately linked with social context and networks. In particular, there is a need to integrate local research, services, prevention and intervention efforts to provide targeted, shared messages. The conference speakers recommended that there be a new focus within youth networks and adult education programs to counter the perception that MDMA is much safer than other drugs. The use of youth-led advocacy and drug prevention programs seems particularly promising for reducing MDMA use among adolescents and young adults.
Four Great Books on Overcoming Addiction:
Support Groups for Addictions:
Additional Resources:
Sources: National Institute of Drug Abuse; See also blogposts in: Addictions: Drug Abuse, and Psychiatry: Addictions: General
Dr. Jeffrey Speller
Dr. Tanya Korkosz
Psychopharmacology Associates of New England
Posted by Dr. Jeff and Dr. Tanya on February 03, 2009 at 07:29 AM in Addictions: Drug Abuse | Permalink | Comments (0)
Many people do not understand why individuals become addicted to drugs or how drugs change the brain to foster compulsive drug abuse. They mistakenly view drug abuse and addiction as strictly a social problem and may characterize those who take drugs as morally weak. One very common belief is that drug abusers should be able to just stop taking drugs if they are only willing to change their behavior. What people often underestimate is the complexity of drug addiction—that it is a disease that impacts the brain and because of that, stopping drug abuse is not simply a matter of willpower. Through scientific advances we now know much more about how exactly drugs work in the brain, and we also know that drug addiction can be successfully treated to help people stop abusing drugs and resume their productive lives.
Drug abuse and addiction are a major burden to society. Estimates of the total overall costs of substance abuse in the United States—including health- and crime-related costs as well as losses in productivity—exceed half a trillion dollars annually. This includes approximately $181 billion for illicit drugs,1 $168 billion for tobacco,2 and $185 billion for alcohol.3 Staggering as these numbers are, however, they do not fully describe the breadth of deleterious public health—and safety—implications, which include family disintegration, loss of employment, failure in school, domestic violence, child abuse, and other crimes.
Addiction
is a chronic, often relapsing brain disease that causes compulsive drug
seeking and use despite harmful consequences to the individual who is
addicted and to those around them. Drug addiction is a brain disease
because the abuse of drugs leads to changes in the structure and
function of the brain. Although it is true that for most people the
initial decision to take drugs is voluntary, over time the changes in
the brain caused by repeated drug abuse can affect a person’s self
control and ability to make sound decisions, and at the same time send
intense impulses to take drugs.
It is because of these changes
in the brain that it is so challenging for a person who is addicted to
stop abusing drugs. Fortunately, there are treatments that help people
to counteract addiction’s powerful disruptive effects and regain
control. Research shows that combining addiction treatment medications,
if available, with behavioral therapy is the best way to ensure success
for most patients. Treatment approaches that are tailored to each
patient’s drug abuse patterns and any co-occurring medical,
psychiatric, and social problems can lead to sustained recovery and a
life without drug abuse.
Similar to other chronic, relapsing
diseases, such as diabetes, asthma, or heart disease, drug addiction
can be managed successfully. And, as with other chronic diseases, it is
not uncommon for a person to relapse and begin abusing drugs again.
Relapse, however, does not signal failure—rather, it indicates that
treatment should be reinstated, adjusted, or that alternate treatment
is needed to help the individual regain control and recover.
Drugs
are chemicals that tap into the brain’s communication system and
disrupt the way nerve cells normally send, receive, and process
information. There are at least two ways that drugs are able to do
this: (1) by imitating the brain’s natural chemical messengers, and/or
(2) by overstimulating the “reward circuit” of the brain.
Some
drugs, such as marijuana and heroin, have a similar structure to
chemical messengers, called neurotransmitters, which are naturally
produced by the brain. Because of this similarity, these drugs are able
to “fool” the brain’s receptors and activate nerve cells to send
abnormal messages.
Other drugs, such as cocaine or
methamphetamine, can cause the nerve cells to release abnormally large
amounts of natural neurotransmitters, or prevent the normal recycling
of these brain chemicals, which is needed to shut off the signal
between neurons. This disruption produces a greatly amplified message
that ultimately disrupts normal communication patterns.
Nearly
all drugs, directly or indirectly, target the brain’s reward system by
flooding the circuit with dopamine. Dopamine is a neurotransmitter
present in regions of the brain that control movement, emotion,
motivation, and feelings of pleasure. The overstimulation of this
system, which normally responds to natural behaviors that are linked to
survival (eating, spending time with loved ones, etc.), produces
euphoric effects in response to the drugs. This reaction sets in motion
a pattern that “teaches” people to repeat the behavior of abusing drugs.
As
a person continues to abuse drugs, the brain adapts to the overwhelming
surges in dopamine by producing less dopamine or by reducing the number
of dopamine receptors in the reward circuit. As a result, dopamine’s
impact on the reward circuit is lessened, reducing the abuser’s ability
to enjoy the drugs and the things that previously brought pleasure.
This decrease compels those addicted to drugs to keep abusing drugs in
order to attempt to bring their dopamine function back to normal. And,
they may now require larger amounts of the drug than they first did to
achieve the dopamine high—an effect known as tolerance.
Long-term
abuse causes changes in other brain chemical systems and circuits as
well. Glutamate is a neurotransmitter that influences the reward
circuit and the ability to learn. When the optimal concentration of
glutamate is altered by drug abuse, the brain attempts to compensate,
which can impair cognitive function. Drugs of abuse facilitate
nonconscious (conditioned) learning, which leads the user to experience
uncontrollable cravings when they see a place or person they associate
with the drug experience, even when the drug itself is not available.
Brain imaging studies of drug-addicted individuals show changes in
areas of the brain that are critical to judgment, decisionmaking,
learning and memory, and behavior control. Together, these changes can
drive an abuser to seek out and take drugs compulsively despite adverse
consequences—in other words, to become addicted to drugs.
No single factor can predict whether or not a person will become addicted to drugs. Risk for addiction is influenced by a person’s biology, social environment, and age or stage of development. The more risk factors an individual has, the greater the chance that taking drugs can lead to addiction. For example:
Drug addiction is a preventable disease. Results from NIDA-funded research have shown that prevention programs that involve families, schools, communities, and the media are effective in reducing drug abuse. Although many events and cultural factors affect drug abuse trends, when youths perceive drug abuse as harmful, they reduce their drug taking. It is necessary, therefore, to help youth and the general public to understand the risks of drug abuse, and for teachers, parents, and healthcare professionals to keep sending the message that drug addiction can be prevented if a person never abuses drugs.
Sources: National Insittute of Mental Health, See also blogposts in: Addictions: Drug Abuse
Dr. Jeffrey Speller
Dr. Tanya Korkosz
Psychopharmacology Associates of New England
Posted by Dr. Jeff and Dr. Tanya on February 03, 2009 at 07:22 AM in Addictions: Drug Abuse | Permalink | Comments (0)
Many substance abuse professionals wonder about the current rate of prescription drug abuse in the United States. An article entitled, “Misuse of prescription drugs is rising in the United States,” published in Medscape (9/8/08) examines this issue. The article reviews a recent report from the Substance Abuse and Mental Health Services Administration. The results of the SAMHSA study were sobering. “Nonmedical use of prescription pain relievers has risen 12% in the past year which included about 67,500 people across the country…Drug use among those aged 55 to 59 years reportedly more than doubled, to 4.1% in 2007. The survey suggests that baby boomers have continued their higher levels of substance abuse as they age.” In addition, “in 2007, adults who had experienced a major depressive episode in the past year were more than twice as likely as other adults to have used drugs (27.4% vs12.8%).” The results of this study suggest that prescription drug abuse and misuse, particularly of prescription pain relievers, are increasing nationwide.
Four Great Books on Overcoming Addiction:
Support Groups for Addictions:
Additional Resources:
Sources: See blogposts in: Addictions: Drug Abuse, and Psychiatry: Addictions: General
Dr. Jeffrey Speller
Dr. Tanya Korkosz
Psychopharmacology Associates of New England
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Posted by Dr. Jeff and Dr. Tanya on October 22, 2008 at 07:37 AM in Addictions: Drug Abuse | Permalink | Comments (0)
Many parents of adolescents are interested in the risk of adolescent prescription drug abuse. An article titled, “Screening Urged to Prevent Prescription Drug Abuse,” published in Psychiatric News (8/15/08), examines this issue. The article reports on a recent study from the Journal of the American Academy of Child and Adolescent Psychiatry, in which researchers surveyed 18,678 adolescents. The results of the study were disturbing: “…one in 12 adolescents aged 12 to 17 (8.2 percent) reported having misused at least one prescription medication in the previous year. This prevalence trailed only the use of alcohol, tobacco, and marijuana. Opioids such as hydrocodone and oxycodone are by far the class of medications most frequently misused by adolescents, followed by stimulants (for example, amphetamines and methylphenidate), tranquilizers (including benzodiazepines and muscle relaxants), and sedatives (for example, barbiturates)…Prescription drug misuse among adolescents was significantly linked to poor academic performance, a major depressive episode in the past year, risk-taking tendencies, a history of mental health treatment in the past year, and the concurrent use of other substances, including cigarettes, alcohol, marijuana, cocaine, or inhalants. Thirty-six percent of these adolescents who misused medications had symptoms that met one or more DSM-IV criteria for substance use disorder…Adolescent girls had a slightly higher prevalence of misusing opioids, stimulants, and tranquilizers than did their male peers.”
The Bottom Line: One in 12 adolescents aged 12 to 17 have misused at least one prescription medication in the past year, most commonly opioids such as hydrocodone (Vicodin) and oxycodone (OxyContin).
Four Great Books on Overcoming Addiction:
Support Groups for Addictions:
Additional Resources:
Sources: See blogposts in: Addictions: Drug Abuse, and Psychiatry: Adolescents and Young Adults
Dr. Jeffrey Speller
Dr. Tanya Korkosz
Psychopharmacology Associates of New England
Posted by Dr. Jeff and Dr. Tanya on September 18, 2008 at 08:46 AM in Addictions: Drug Abuse, Psychiatry: Adolescents and Young Adults | Permalink | Comments (0)
Mental health professionals with an interest in addictions have wondered about the effectiveness of buprenorphine as compared to naltrexone in the treatment of heroin addicts. An article titled, “Buprenorphine Bests Naltrexone in Treating Heroin Addicts,” published in Psychiatric News (8/15/08), examines this issue. The article reports on a recent Lancet study in which the researchers studied 126 heroin addicts, each of whom was assigned to one of three treatment groups: buprenorphine, naltrexone, or placebo. The results were interesting. Those treated with buprenorphine had significantly longer duration of abstinence before the first heroin use (positive urine test) and duration to heroin-related relapse (three consecutive opioid-positive urine tests) than those who received naltrexone or placebo (see chart). The buprenorphine-treated group also had significantly better outcome than the placebo group in the maximum number of consecutive days of abstinence.”
The Bottom Line: This study
suggests that buprenorphine may be superior to naltrexone in the treatment of
heroin addicts.
Reference: Original Article
Four Great Books on Overcoming Addiction:
Support Groups for Addictions:
Dr. Jeffrey Speller
Dr. Tanya Korkosz
Psychopharmacology Associates of New England
Posted by Dr. Jeff and Dr. Tanya on September 17, 2008 at 09:16 AM in Addictions: Drug Abuse | Permalink | Comments (0)