Alcoholism & Drug Abuse Weekly
Volume 23 Number 33
August 29, 2011
ASAM admits error in omitting NIAAA in definition publicity
In announcing its new broader definition of addiction to include non-substance addictions such as sex and gambling (see ADAW, August 22), the American Society of Addiction Medicine (ASAM) made an almost fatal error. It treated alcohol like an afterthought and pointedly omitted any mention of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) while suggesting — incorrectly, as it turns out — that the National Institute on Drug Abuse (NIDA) was involved in crafting the definition, ADAW has learned.
ASAM past president Michael Miller, M.D., told ADAW last week that nobody from NIDA was involved officially in the process leading to release of the definition. “The press release did not state things in a clear manner and clearly led people to believe that we had some kind of formal connection with NIDA,” Miller said.
It strains belief for some leaders, however, to think that ASAM physicians were not aware of the bitter struggle between NIDA and NIAAA
researchers over the upcoming merger of the institutes, which will create a new, single institute of addiction — a merger NIDA supported
and NIAAA opposed. NIAAA officials were furious when the definition — and the press release — came out, published August 15 on the ASAM website.
“We recognize that ASAM is extremely important to physicians who are specializing in substance use disorders,” said Howard B. Moss, M.D., associate director for clinical and translational research at NIAAA. “But we are concerned that the narrow definitional focus on neuroscience
doesn’t really address the psychological and sociocultural aspects of addiction,” he told ADAW. “We view it as reductionist.”
Moss also said the timing of the definition’s release was awkward, since the DSM-5 process is taking place at the same time. “DSM will
have definitions that will be discussed in the diagnostic criteria,” he said. And finally, calling addiction a disease is hardly new.
NIAAA is also very concerned about binge drinking, underage alcohol use, and drinking and driving — problems that aren’t necessarily facets
of addictive disorders, said Moss.
“We met with NIAAA to explain to them how sorry we are that we did not vet this with them more officially,” ASAM’s Miller said. “They
are at least embarrassed and extremely disappointed because they were blindsided with people coming to them with questions about
things they haven’t even seen.”
When we talked to Miller last week, no decision had yet been made about whether ASAM would publicize a correction about NIDA/
NIAAA involvement. But, he said, “We have apologized to NIAAA very publicly.”
NIAAA is “not aware of any public apology,” according to a NIAAA press officer.
Sensitivity issues
Miller blamed some of the “lack of sensitivity” to the fact that ASAM has a new CEO and a new staffer in charge of communications. “ASAM
has learned through this process that it must be much more sensitive to these delicate differences of the two institutes, and that so many
people are looking for messages in the tea leaves that may not be there.”
ASAM has “no official position” on the proposed merger of the institutes, said Miller.
Sources at NIAAA said people there are “absolutely furious.” They believe that ASAM is saying — just as the pro-merger researchers had
said — that all neurochemical pathways to addiction are the same. In fact, they say, alcohol is not the same — it goes everywhere in the
brain. There is no alcohol receptor, said Moss.
Not diagnostic criteria
The ASAM definition is just that — it is not diagnostic criteria, and it can’t be used for diagnosis, said Miller. That is the province of the
American Psychiatric Association (APA), which field-tests its criteria.
ASAM really wanted to update its definition because the organization had two different definitions out there — one that applies only to alcoholism
and that dates back to 1990, and one for addiction that was created in 2001 in collaboration with the American Pain Society, Miller said. “These two did not align, there were subtle differences,” he said. So the new definition eliminated the old definition of alcoholism and added various “process” addictions.
“We did get some cautionary advice from different quarters,” said Miller. For example, alcoholism researcher Carlton Erickson “blasted the whole project,” said Miller. Erickson suggested not to talk about spirituality or non-substance addictions, but to “stick to what is known,” recalled Miller. But in general there was consensus, he said.
“Most clinicians said this makes sense, and the board of directors of ASAM unanimously approved it,” said Miller.
Friday, August 26, 2011
Sunday, August 21, 2011
Back for more!
I think I'm ready to again take up my lance and tilt at the windmill of changing the paradigm of treatment in this country (if not everywhere!) I haven't been posting mostly because I've been overwhelmed with the realities of trying to earn a living seeing patients in a heavily managed care environment. I've learned a lot, some of it quite painfully. I think in the long run it will serve me, and hopefully others, well, because this is a harsh, difficult and treacherous environment. I understand much better why physicians avoid particularly challenging patients, and why they are so conservative in their approach. Everyone is overwhelmed. There are so many patients we really don't have any treatment for or even understand what is wrong with them. It feels like we are putting Band-Aids on gaping infected wounds and sending people out the door. Many are simply left to cope on their own. All of this has been exacerbated by the Great Recession, which is wreaking havoc on anyone but the wealthy, and by a system of care heavily dominated by procedure-oriented specialty care rather than compassionate, comprehensive care. One reason for feeling overwhelmed is that it all seems so well, overwhelming. How can anyone hope to change this terribly dysfunctional system? Lately I've adopted the strategy of focusing on smaller, more achievable goals. This fall I will start seeing more patients in private practice and fewer in a managed care setting. I hope to build on this seedling to establish the first ALLTYR Clinic. Wish me luck.
Monday, May 9, 2011
Opioids for Treatment Resistant Depression?
My colleague, Mark Rose, recently submitted this post about the potential use of buprenorphine as an antidepressant treatment for treatment resistant depression. To our knowledge, no further studies of this have been done. Perhaps it's time?
MW
Buprenorphine may be effective in treatment-refractory depression
Mark E. Rose, MA
Licensed Psychologist
Persons with major depressive disorder (MDD) are considered treatment-refractory (TRD) when they fail to respond to multiple trials of antidepressant medication from different classes (Keller 2005). TRD is a devastating condition that results in substantial health care and economic cost, and untold suffering to the patient and family members (Nierenberg et al. 2007). Most FDA-approved antidepressant drugs act through monoamine reuptake inhibition, and medications that act through alternate mechanisms need to be available to patients with unrelenting depression that is untreatable with conventional antidepressants. The results of a study published 15 years ago hint that a currently available drug may provide greater benefit to patients with TRD than any other known pharmaceutical agent.
Although opioids were used to treat MDD until the late 1950s, research evaluating their antidepressant potential has been very rare in the past 60 years (Berrocoso et al. 2009). The synthetic opioid buprenorphine is a partial mu receptor agonist and kappa receptor antagonist, is exceptionally safe in overdose, and produces substantially less euphoria than pure mu receptor agonists such as morphine and oxycodone. A small study (Bodkin et al. 1995) evaluated the therapeutic potential of buprenorphine in the treatment of TRD. The 10 study participants averaged a 20.7–year duration of unipolar major depression, 7.6 previous unsuccessful antidepressant trials, and a HAM-D score of 28.1. Buprenorphine was initiated in open-label manner at 0.15 mg/d with maximum upward titration to 1.80 mg/d over the 4-6 week trial (final mean dose 1.26 mg/d). Three subjects dropped out due to malaise, nausea, and dysphoria. Of the remaining 7 subjects, 6 achieved marked clinical improvement. The mean endpoint HAM-D score was 10.7, a 60.7% reduction from baseline, and 4 patients achieved complete remission (HAM-D ≤ 6). The mean overall level of functioning increased 45.5% and mean subjective depression rating decreased 50%. Significant improvement became apparent at the end of week 1.
The authors conclude that the results are remarkable, with the number of previous treatment failures, the level of disease severity, and the duration of improvement arguing against placebo effect as the basis of treatment response. Patients did not report euphoria or intoxication but instead felt ‘more normal’, which together with the 33% drop-out suggest limited abuse liability in persons with TRD. These results are literally begging for replication, but sadly, despite awareness of this data for 15 years, researchers have not conducted follow-up studies due to the stigma surrounding opioid drugs and their association with addiction.
Keller MB. Issues in treatment-resistant depression. J Clin Psychiatry. 2005;66(Suppl 8):5-12.
Nierenberg AA, Katz J, Fava M. A critical overview of the pharmacologic
management of treatment-resistant depression. Psychiatr Clin North Am. 2007;30(1):13-29.
Berrocoso E, et al. Opiates as antidepressants. Current Pharmaceutical Design. 2009;15:1612-1622.
Bodkin JA, Zornberg GL, Lukas SE, Cole JO. Buprenorphine treatment of refractory depression. J Clin Psychopharmacol. 1995;15:49-57.
MW
Buprenorphine may be effective in treatment-refractory depression
Mark E. Rose, MA
Licensed Psychologist
Persons with major depressive disorder (MDD) are considered treatment-refractory (TRD) when they fail to respond to multiple trials of antidepressant medication from different classes (Keller 2005). TRD is a devastating condition that results in substantial health care and economic cost, and untold suffering to the patient and family members (Nierenberg et al. 2007). Most FDA-approved antidepressant drugs act through monoamine reuptake inhibition, and medications that act through alternate mechanisms need to be available to patients with unrelenting depression that is untreatable with conventional antidepressants. The results of a study published 15 years ago hint that a currently available drug may provide greater benefit to patients with TRD than any other known pharmaceutical agent.
Although opioids were used to treat MDD until the late 1950s, research evaluating their antidepressant potential has been very rare in the past 60 years (Berrocoso et al. 2009). The synthetic opioid buprenorphine is a partial mu receptor agonist and kappa receptor antagonist, is exceptionally safe in overdose, and produces substantially less euphoria than pure mu receptor agonists such as morphine and oxycodone. A small study (Bodkin et al. 1995) evaluated the therapeutic potential of buprenorphine in the treatment of TRD. The 10 study participants averaged a 20.7–year duration of unipolar major depression, 7.6 previous unsuccessful antidepressant trials, and a HAM-D score of 28.1. Buprenorphine was initiated in open-label manner at 0.15 mg/d with maximum upward titration to 1.80 mg/d over the 4-6 week trial (final mean dose 1.26 mg/d). Three subjects dropped out due to malaise, nausea, and dysphoria. Of the remaining 7 subjects, 6 achieved marked clinical improvement. The mean endpoint HAM-D score was 10.7, a 60.7% reduction from baseline, and 4 patients achieved complete remission (HAM-D ≤ 6). The mean overall level of functioning increased 45.5% and mean subjective depression rating decreased 50%. Significant improvement became apparent at the end of week 1.
The authors conclude that the results are remarkable, with the number of previous treatment failures, the level of disease severity, and the duration of improvement arguing against placebo effect as the basis of treatment response. Patients did not report euphoria or intoxication but instead felt ‘more normal’, which together with the 33% drop-out suggest limited abuse liability in persons with TRD. These results are literally begging for replication, but sadly, despite awareness of this data for 15 years, researchers have not conducted follow-up studies due to the stigma surrounding opioid drugs and their association with addiction.
Keller MB. Issues in treatment-resistant depression. J Clin Psychiatry. 2005;66(Suppl 8):5-12.
Nierenberg AA, Katz J, Fava M. A critical overview of the pharmacologic
management of treatment-resistant depression. Psychiatr Clin North Am. 2007;30(1):13-29.
Berrocoso E, et al. Opiates as antidepressants. Current Pharmaceutical Design. 2009;15:1612-1622.
Bodkin JA, Zornberg GL, Lukas SE, Cole JO. Buprenorphine treatment of refractory depression. J Clin Psychopharmacol. 1995;15:49-57.
Thursday, May 5, 2011
Research Study Results: Skepticism Required!
This new study identified some functional neuroimaging correlates to performance on a task that measures something called "delay discounting." This now highly popular test (among scientists) gives people a choice or series of choices that boils down to this question: "Do you want a smaller reward (typically money) sooner, or a larger reward later?" For example, a subject might be asked to decide between getting $1 right now, or getting $20 in two weeks. "Delay discounting" refers to discounting the value of a future reward, thus increasing the likelihood of choosing the smaller reward sooner. While there have been many such studies, I'm posting this one because of the comments made by Dan Hommer at the National Institute on Alcohol Abuse and Alcoholism. His comments focus on the concept of "impulsivity." As it turns out, there is no gold standard for measuring this construct, nor is there any consensus about what it means in more than general terms. The same holds true for many other terms used in imaging and other studies, including reward, behavioral inhibition and disinhibition, liking, wanting, attention and so forth. Bottom line: read or listen to the results of studies like this skeptically. Remember that scientists and media professionals want something to be newsworthy, leading to inflation of the importance and clarity of much research.
MW
Researchers Link Alcohol-Dependence Impulsivity to Brain Anomalies
ScienceDaily
May 1, 2011
Researchers already know that alcohol dependence (AD) is strongly associated with impaired impulse control or, more precisely, the inability to choose large, delayed rewards rather than smaller but more immediate rewards. Findings from a study using functional magnetic resonance imaging (fMRI) to investigate the neural basis of impulsive choice among individuals with alcohol use disorders (AUDs) suggest that impulsive choice in AD may be the result of functional anomalies in widely distributed but interconnected brain regions that are involved in cognitive and emotional control.
Results will be published in the July 2011 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"Individuals with AD score higher on questionnaires that measure impulsivity -- for example, 'I act without thinking' -- are less able to delay gratification, and are less able to inhibit responses," said Eric D. Claus, a research scientist with The Mind Research Network and first author of the study.
Given that impulsive choice in AUDs has been associated with impairment of frontal cortical systems involved in behavioral control, Claus explained, this study was designed to examine the neural correlates of one specific aspect of impulsivity, the ability to delay immediate gratification and instead choose rewards in the future.
"We investigated this choice process in individuals with alcohol use problems ranging from alcohol abuse to severe AD that required treatment," said Claus. "This is the largest study to date that has investigated the neural correlates of impulsive choice in AD, which enabled us to examine the full range of AUDs instead of only examining extreme group differences."
Claus and his colleagues examined 150 individuals (103 males, 47 females) with various degrees of alcohol use. All of the participants completed a delay discounting task -- during which two options were presented, a small monetary (e.g., $10) reward available immediately or a larger monetary reward (e.g., $30) available in time (e.g., two weeks) -- while undergoing fMRI. Impulsive choice was defined as the selection of the more immediate option.
"We showed two things," said Claus. "We replicated previous research by showing that AUD severity was associated with a greater tendency to discount future rewards. In addition, we showed that when individuals with more severe AUDs did delay gratification, they engaged the insula and supplementary motor area -- regions involved in emotional processing and response conflict -- to a greater degree than individuals with less severe AUDs. In summary, these findings suggest that the dysfunction in these regions is graded and increases as a function of AUD severity, rather than operating as an all-or-none function."
"This work showed that the brains of alcoholics don't behave all that differently from the brains of non-alcoholics during delay discounting but that the alcoholic brain had to work harder when they chose the delayed reward," said Daniel W. Hommer, chief of the Section of Brain Electrophysiology & Imaging at the National Institute on Alcohol Abuse and Alcoholism. "Many different studies have shown similar results, that is, alcoholics have a greater increase in brain blood flow to perform the same task as non-alcoholics."
"The current study suggests that the neural dysfunction underlying impulsive choice seems to increase with AD severity," added Claus. "Now that we know that this neural dysfunction is associated with impulsivity, the next steps are to determine whether this impulsivity predates the onset of AD and whether neural measures of impulsivity can predict who will respond best to particular types of treatment. Further, the particular neural dysfunction that we observed indicates that individuals with more AD may be more impulsive because their brain is aversive to delay gratification, and not because it is rewarding to be impulsive. Clinicians might need to deal directly with the aversion of choosing future benefits over immediate ones."
"The most important thing about this paper is that it leads you to question what people mean by impulsive behavior and how should it be measured," said Hommer. "The field has defined increased discounting of time -- failure to delay gratification -- as a good measure of impulsiveness, but the results reported in this paper say 'Wait a minute, delay discounting does not correspond to what is usually meant by impulsiveness.' Rather, brain activity during a delay discounting task looks more like how the brain responds during conflicted decision-making than it does during rapid, unconflicted choice of a highly valued goal." Hommer added that this sort of debate is important to researchers, forcing them to think more carefully about what they mean by impulsive choice.
MW
Researchers Link Alcohol-Dependence Impulsivity to Brain Anomalies
ScienceDaily
May 1, 2011
Researchers already know that alcohol dependence (AD) is strongly associated with impaired impulse control or, more precisely, the inability to choose large, delayed rewards rather than smaller but more immediate rewards. Findings from a study using functional magnetic resonance imaging (fMRI) to investigate the neural basis of impulsive choice among individuals with alcohol use disorders (AUDs) suggest that impulsive choice in AD may be the result of functional anomalies in widely distributed but interconnected brain regions that are involved in cognitive and emotional control.
Results will be published in the July 2011 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"Individuals with AD score higher on questionnaires that measure impulsivity -- for example, 'I act without thinking' -- are less able to delay gratification, and are less able to inhibit responses," said Eric D. Claus, a research scientist with The Mind Research Network and first author of the study.
Given that impulsive choice in AUDs has been associated with impairment of frontal cortical systems involved in behavioral control, Claus explained, this study was designed to examine the neural correlates of one specific aspect of impulsivity, the ability to delay immediate gratification and instead choose rewards in the future.
"We investigated this choice process in individuals with alcohol use problems ranging from alcohol abuse to severe AD that required treatment," said Claus. "This is the largest study to date that has investigated the neural correlates of impulsive choice in AD, which enabled us to examine the full range of AUDs instead of only examining extreme group differences."
Claus and his colleagues examined 150 individuals (103 males, 47 females) with various degrees of alcohol use. All of the participants completed a delay discounting task -- during which two options were presented, a small monetary (e.g., $10) reward available immediately or a larger monetary reward (e.g., $30) available in time (e.g., two weeks) -- while undergoing fMRI. Impulsive choice was defined as the selection of the more immediate option.
"We showed two things," said Claus. "We replicated previous research by showing that AUD severity was associated with a greater tendency to discount future rewards. In addition, we showed that when individuals with more severe AUDs did delay gratification, they engaged the insula and supplementary motor area -- regions involved in emotional processing and response conflict -- to a greater degree than individuals with less severe AUDs. In summary, these findings suggest that the dysfunction in these regions is graded and increases as a function of AUD severity, rather than operating as an all-or-none function."
"This work showed that the brains of alcoholics don't behave all that differently from the brains of non-alcoholics during delay discounting but that the alcoholic brain had to work harder when they chose the delayed reward," said Daniel W. Hommer, chief of the Section of Brain Electrophysiology & Imaging at the National Institute on Alcohol Abuse and Alcoholism. "Many different studies have shown similar results, that is, alcoholics have a greater increase in brain blood flow to perform the same task as non-alcoholics."
"The current study suggests that the neural dysfunction underlying impulsive choice seems to increase with AD severity," added Claus. "Now that we know that this neural dysfunction is associated with impulsivity, the next steps are to determine whether this impulsivity predates the onset of AD and whether neural measures of impulsivity can predict who will respond best to particular types of treatment. Further, the particular neural dysfunction that we observed indicates that individuals with more AD may be more impulsive because their brain is aversive to delay gratification, and not because it is rewarding to be impulsive. Clinicians might need to deal directly with the aversion of choosing future benefits over immediate ones."
"The most important thing about this paper is that it leads you to question what people mean by impulsive behavior and how should it be measured," said Hommer. "The field has defined increased discounting of time -- failure to delay gratification -- as a good measure of impulsiveness, but the results reported in this paper say 'Wait a minute, delay discounting does not correspond to what is usually meant by impulsiveness.' Rather, brain activity during a delay discounting task looks more like how the brain responds during conflicted decision-making than it does during rapid, unconflicted choice of a highly valued goal." Hommer added that this sort of debate is important to researchers, forcing them to think more carefully about what they mean by impulsive choice.
Monday, May 2, 2011
Evidence Stronger for Cannabis-Psychosis Link
I've been a skeptic about the potential role of cannabis as an independent risk factor for developing psychosis, but this new study addresses some of the weaknesses of previous studies and shows a strong association between persistent cannabis use and the later development of psychosis. They only studied cannabis use that started after the study baseline to eliminate the effects of preexisting use, and they excluded anyone at baseline with any psychotic symptoms. The authors suggest that the risk might involve increasing the persistence of subclinical psychotic phenomena that would otherwise be transient, an interesting hypothesis. Underlying that suggestion is recent evidence that psychotic phenomena exist along a continuum from minor transient symptoms (quite common) to persistent and then more severe symptoms. Also note that the risk associated with cannabis was independent of family history of psychosis. There are still many unanswered questions about this link, but the evidence for it is growing and is strong enough now that warning parents and adolescents is probably warranted. Here's the link to the article.
MW
BMJ 2011; 342:d738
Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study
OPEN ACCESS
Rebecca Kuepper, research psychologist1, Jim van Os, professor1, visiting professor2, Roselind Lieb, professor34, Hans-Ulrich Wittchen, professor45, Michael Höfler, research statistician5, Cécile Henquet, lecturer1
+ Author Affiliations
1Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Center, Maastricht, Netherlands
2King’s College London, King’s Health Partners, Department of Psychosis Studies, Institute of Psychiatry, London, UK
3Department of Psychology, Division of Epidemiology and Health Psychology, University of Basel, Switzerland
4Max Planck Institute of Psychiatry, Munich, Germany
5Institute of Clinical Psychology and Psychotherapy, Technical University Dresden, Germany
Correspondence to: J van Os, Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Center, PO Box 616, NL-6200 MD, Maastricht, Netherlands j.vanos@sp.unimaas.nl
Accepted 31 December 2010
Abstract
Objective To determine whether use of cannabis in adolescence increases the risk for psychotic outcomes by affecting the incidence and persistence of subclinical expression of psychosis in the general population (that is, expression of psychosis below the level required for a clinical diagnosis).
Design Analysis of data from a prospective population based cohort study in Germany (early developmental stages of psychopathology study).
Setting Population based cohort study in Germany.
Participants 1923 individuals from the general population, aged 14-24 at baseline.
Main outcome measure Incidence and persistence of subthreshold psychotic symptoms after use of cannabis in adolescence. Cannabis use and psychotic symptoms were assessed at three time points (baseline, T2 (3.5 years), T3 (8.4 years)) over a 10 year follow-up period with the Munich version of the composite international diagnostic interview (M-CIDI).
Results In individuals who had no reported lifetime psychotic symptoms and no reported lifetime cannabis use at baseline, incident cannabis use over the period from baseline to T2 increased the risk of later incident psychotic symptoms over the period from T2 to T3 (adjusted odds ratio 1.9, 95% confidence interval 1.1 to 3.1; P=0.021). Furthermore, continued use of cannabis increased the risk of persistent psychotic symptoms over the period from T2 to T3 (2.2, 1.2 to 4.2; P=0.016). The incidence rate of psychotic symptoms over the period from baseline to T2 was 31% (152) in exposed individuals versus 20% (284) in non-exposed individuals; over the period from T2 to T3 these rates were 14% (108) and 8% (49), respectively.
Conclusion Cannabis use is a risk factor for the development of incident psychotic symptoms. Continued cannabis use might increase the risk for psychotic disorder by impacting on the persistence of symptoms
MW
BMJ 2011; 342:d738
Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study
OPEN ACCESS
Rebecca Kuepper, research psychologist1, Jim van Os, professor1, visiting professor2, Roselind Lieb, professor34, Hans-Ulrich Wittchen, professor45, Michael Höfler, research statistician5, Cécile Henquet, lecturer1
+ Author Affiliations
1Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Center, Maastricht, Netherlands
2King’s College London, King’s Health Partners, Department of Psychosis Studies, Institute of Psychiatry, London, UK
3Department of Psychology, Division of Epidemiology and Health Psychology, University of Basel, Switzerland
4Max Planck Institute of Psychiatry, Munich, Germany
5Institute of Clinical Psychology and Psychotherapy, Technical University Dresden, Germany
Correspondence to: J van Os, Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Center, PO Box 616, NL-6200 MD, Maastricht, Netherlands j.vanos@sp.unimaas.nl
Accepted 31 December 2010
Abstract
Objective To determine whether use of cannabis in adolescence increases the risk for psychotic outcomes by affecting the incidence and persistence of subclinical expression of psychosis in the general population (that is, expression of psychosis below the level required for a clinical diagnosis).
Design Analysis of data from a prospective population based cohort study in Germany (early developmental stages of psychopathology study).
Setting Population based cohort study in Germany.
Participants 1923 individuals from the general population, aged 14-24 at baseline.
Main outcome measure Incidence and persistence of subthreshold psychotic symptoms after use of cannabis in adolescence. Cannabis use and psychotic symptoms were assessed at three time points (baseline, T2 (3.5 years), T3 (8.4 years)) over a 10 year follow-up period with the Munich version of the composite international diagnostic interview (M-CIDI).
Results In individuals who had no reported lifetime psychotic symptoms and no reported lifetime cannabis use at baseline, incident cannabis use over the period from baseline to T2 increased the risk of later incident psychotic symptoms over the period from T2 to T3 (adjusted odds ratio 1.9, 95% confidence interval 1.1 to 3.1; P=0.021). Furthermore, continued use of cannabis increased the risk of persistent psychotic symptoms over the period from T2 to T3 (2.2, 1.2 to 4.2; P=0.016). The incidence rate of psychotic symptoms over the period from baseline to T2 was 31% (152) in exposed individuals versus 20% (284) in non-exposed individuals; over the period from T2 to T3 these rates were 14% (108) and 8% (49), respectively.
Conclusion Cannabis use is a risk factor for the development of incident psychotic symptoms. Continued cannabis use might increase the risk for psychotic disorder by impacting on the persistence of symptoms
Friday, April 22, 2011
Addiction: A Potentially Fatal Behavioral Disease
A few months ago, an article in the St. Paul Pioneer Press described a "wet house," where people who were unable to stop drinking were able to get housing and access to services without requiring that they stop drinking. A very typical response, especially from people in 12-step programs and in treatment programs, was that this was "giving up" on these unfortunate individuals, that the proper treatment or 12-step participation would result in their being able to sustain abstinence. A number of people have asked me about this. Here's my response to a recent inquiry.
MW
I actually did research on this in the late 1980s and got quite deep into what the best approach was for chronic public inebriates. The problem we were trying to address was that these folks would cycle through the detox center over and over. A minority of users accounted for the majority of visits to detox, which is expensive. In addition they are frequent guests in emergency rooms and hospitals. Here's what we found:
1. Many of them were using detox as a shelter. They were homeless, couldn't maintain a home, and shelters wouldn't take anyone who appeared to be drinking. Some of them would drink a little alcohol and fall down in front of a police car to get transported to detox.
2. For about 1/2 of them, a case manager was able to work with them and get them housed and help them with their food purchases, housekeeping, money management and so forth. This group saw dramatic drops in detox and emergency room usage.
3. The other half were so damaged from their early lives (including many American Indians who were dependent before age 12, and grew up in chaotic environments) that they couldn't form a helping relationship with a case manager. For this group there was nothing we could do to help. Trying to coerce them (e.g., attempt to get control of their disability payments) was counterproductive.
4. All in all providing housing even though people kept drinking was highly cost effective and resulted in better health for the individuals.
There is a similar place in Minneapolis and I know of one in Portland, possibly Seattle.
Here's the sad fact: a small proportion of people with alcohol or drug dependence are unable to quit and will die of their disease. After decades of working with them, I have concluded that any of them would quit drinking or using if they could. Most make multiple efforts. We accept that heart disease, neurological disease and cancer often lead to death in spite of our best efforts and treatments. We have trouble accepting that there are fatal behavioral diseases. This is because we don't think of the brain as an organ. What happens when this organ gets dysfunctional, cannot do its normal job of regulating thinking, feeling, perception, memory, communication, and most importantly here, behavior? Severe, progressive addiction is a result of multiple social, personal, and genetic factors, but the end result is that the individual loses control over their behavior, much like the diabetic loses control of her blood sugar. If you reflect on it, most of our behavior is regulated by unconscious processes that are automatic. It is difficult under good conditions to alter that. Think of smoking, exercise, diet, aggression, how we behave towards our spouses or boss. Our (rational, deliberate) control over our behavior is at best partial. How often do we do something when we are angry that we regret later? Don't all of us have repetitive behavior patterns that are clearly dysfunctional but persist in spite of our best efforts to change them? An example: the fall of Elliot Spitzer, governor of New York, who got caught with a stripper. This was not a rational decision on his part. Another: President Bill Clinton, whose compulsive sexual behavior destroyed his second term.
In addiction, the brain loses the ability to regulate behavior relative to a specific intoxicant. In really severe addiction this loss of control may lead to death. I think that people in this situation are horrified at what is happening to them and terrified that they can't stop it. I've never met an addict who liked being addicted. (They want intoxication, but not addiction.)
In the 1990s, there was a group of us in Minnesota who regularly met to discuss what the optimal approach was to helping public inebriates. We examined everything from locking them up in the state hospital (which is what used to be done), to case management, housing, offering medical and psychiatric services, etc. We concluded that having a safe place for people to live when they can't stop drinking was the best overall solution, most cost effective, most protective of human rights, and most humane.
The idea that someone can stop if they really want to, or if they really work a 12 step program, is a terrible thing. It's not true. Why would brain dysregulation be 100% curable merely by the individual wanting it to be so? We blame obese people for their problems, we blame people who get heart disease for eating too many hamburgers and not exercising enough, we blame people with cancer for not doing the right preventive thing. We do this because it protects us from the terrifying reality that these things occur in spite of everything we can do to prevent them, that our own behavior is not well controlled, that our environment is often responsible for our predicament, or worst of all that it's simply a gene-environment interaction over which we are powerless.
There are many other potentially fatal behavioral disorders, including antisocial personality disorder (death from violence,) anorexia nervosa, depression (suicide,) schizophrenia (suicide, heavy smoking,) obesity and lack of exercise (the second most important cause of preventable mortality,) reckless or distracted driving or speeding, overwork and sleep deprivation, post traumatic stress disorder (suicide, addiction, violence,) uncontrolled aggression (assault and murder,) and addiction to pain killers and sedatives (unintentional overdose.)
I have (clinically) stayed with many people as they died of their addiction. I didn't abandon them because they "didn't get the program" or "didn't really want to get sober." They all did, desperately. But they couldn't. And I couldn't help them. And they died.
MW
I actually did research on this in the late 1980s and got quite deep into what the best approach was for chronic public inebriates. The problem we were trying to address was that these folks would cycle through the detox center over and over. A minority of users accounted for the majority of visits to detox, which is expensive. In addition they are frequent guests in emergency rooms and hospitals. Here's what we found:
1. Many of them were using detox as a shelter. They were homeless, couldn't maintain a home, and shelters wouldn't take anyone who appeared to be drinking. Some of them would drink a little alcohol and fall down in front of a police car to get transported to detox.
2. For about 1/2 of them, a case manager was able to work with them and get them housed and help them with their food purchases, housekeeping, money management and so forth. This group saw dramatic drops in detox and emergency room usage.
3. The other half were so damaged from their early lives (including many American Indians who were dependent before age 12, and grew up in chaotic environments) that they couldn't form a helping relationship with a case manager. For this group there was nothing we could do to help. Trying to coerce them (e.g., attempt to get control of their disability payments) was counterproductive.
4. All in all providing housing even though people kept drinking was highly cost effective and resulted in better health for the individuals.
There is a similar place in Minneapolis and I know of one in Portland, possibly Seattle.
Here's the sad fact: a small proportion of people with alcohol or drug dependence are unable to quit and will die of their disease. After decades of working with them, I have concluded that any of them would quit drinking or using if they could. Most make multiple efforts. We accept that heart disease, neurological disease and cancer often lead to death in spite of our best efforts and treatments. We have trouble accepting that there are fatal behavioral diseases. This is because we don't think of the brain as an organ. What happens when this organ gets dysfunctional, cannot do its normal job of regulating thinking, feeling, perception, memory, communication, and most importantly here, behavior? Severe, progressive addiction is a result of multiple social, personal, and genetic factors, but the end result is that the individual loses control over their behavior, much like the diabetic loses control of her blood sugar. If you reflect on it, most of our behavior is regulated by unconscious processes that are automatic. It is difficult under good conditions to alter that. Think of smoking, exercise, diet, aggression, how we behave towards our spouses or boss. Our (rational, deliberate) control over our behavior is at best partial. How often do we do something when we are angry that we regret later? Don't all of us have repetitive behavior patterns that are clearly dysfunctional but persist in spite of our best efforts to change them? An example: the fall of Elliot Spitzer, governor of New York, who got caught with a stripper. This was not a rational decision on his part. Another: President Bill Clinton, whose compulsive sexual behavior destroyed his second term.
In addiction, the brain loses the ability to regulate behavior relative to a specific intoxicant. In really severe addiction this loss of control may lead to death. I think that people in this situation are horrified at what is happening to them and terrified that they can't stop it. I've never met an addict who liked being addicted. (They want intoxication, but not addiction.)
In the 1990s, there was a group of us in Minnesota who regularly met to discuss what the optimal approach was to helping public inebriates. We examined everything from locking them up in the state hospital (which is what used to be done), to case management, housing, offering medical and psychiatric services, etc. We concluded that having a safe place for people to live when they can't stop drinking was the best overall solution, most cost effective, most protective of human rights, and most humane.
The idea that someone can stop if they really want to, or if they really work a 12 step program, is a terrible thing. It's not true. Why would brain dysregulation be 100% curable merely by the individual wanting it to be so? We blame obese people for their problems, we blame people who get heart disease for eating too many hamburgers and not exercising enough, we blame people with cancer for not doing the right preventive thing. We do this because it protects us from the terrifying reality that these things occur in spite of everything we can do to prevent them, that our own behavior is not well controlled, that our environment is often responsible for our predicament, or worst of all that it's simply a gene-environment interaction over which we are powerless.
There are many other potentially fatal behavioral disorders, including antisocial personality disorder (death from violence,) anorexia nervosa, depression (suicide,) schizophrenia (suicide, heavy smoking,) obesity and lack of exercise (the second most important cause of preventable mortality,) reckless or distracted driving or speeding, overwork and sleep deprivation, post traumatic stress disorder (suicide, addiction, violence,) uncontrolled aggression (assault and murder,) and addiction to pain killers and sedatives (unintentional overdose.)
I have (clinically) stayed with many people as they died of their addiction. I didn't abandon them because they "didn't get the program" or "didn't really want to get sober." They all did, desperately. But they couldn't. And I couldn't help them. And they died.
Monday, April 18, 2011
Ideology, Attitude and Science: Buyer Beware!
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.
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.
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