Paula Riggs, PhD, Professor of Psychiatry, notes the most recent Monitoring the Future Survey shows a significant increase in marijuana use, including daily marijuana use among U. S. high school students and a decrease in perceived risk of use. “There are a number of indicators, including the increasing number of states that have passed ‘medical marijuana’ legislation, and that society as a whole tends to view marijuana as a relatively benign, recreational drug. However, scientific research does not support this.”

A growing body of research shows that adolescent marijuana use can be detrimental to the brain development and may produce long-lasting neurocognitive deficits and increased risk of mental health problems including psychosis, said Dr. Riggs, who spoke about this topic at the recent California Society of Addiction Medicine meeting.

Marijuana is the most commonly used illicit drug in the United States. Although some have questioned whether marijuana is an addictive drug, scientific research shows that one in 10 people overall, and one in six adolescents, who use marijuana develop dependence or addiction, Dr. Riggs says. Research shows that marijuana can cause structural damage, neuronal loss and impair brain function on a number of levels, from basic motor coordination to more complex tasks, such as the ability to plan, organize, solve problems, remember, make decisions and control behavior and emotions.

Dr. Riggs also cited recent studies indicating that adolescents may be more vulnerable to addiction, in part due to rapid brain development. “Emerging research suggests that individuals who start using marijuana during their teenage years may have longer-lasting cognitive impairments in executive functioning than those who start later,” she says. “Animal studies also suggest that exposure to marijuana during adolescence compared to adulthood may increase the vulnerability or risk of developing addiction to other substances of abuse such as cocaine and methamphetamine.”

She adds, “It is important for pediatricians, psychiatrists and other mental health clinicians to be aware of current research because they are on the front line to identify teens when they first start to experiment. They need to be able to effectively screen adolescents for marijuana use, and be armed with the scientific facts to educate teens and families about associated risks.”

Source   www.partnershipatdrugfree.org  Nov. 2011

Simon Jones/Science/AAAS

The red areas show gray matter that
is abnormally increased in drug users. Blue shows gray matter that is
abnormally decreased in drug users. Yellow shows white matter tracts, called
fractional anisotropy or FA. FA is significantly reduced in both the drug users
and in their siblings, which suggests that the white matter tracts work less
efficiently.

Many addicts inherit a brain that has trouble just saying
no to drugs.

A study
in Science finds that cocaine addicts have abnormalities in
areas of the brain involved in self-control. And these abnormalities appear to predate
any drug abuse.

The study, done by a team at the University
of Cambridge in the U.K., looked at
50 pairs of siblings. One member of each pair was a cocaine addict. The other
had no history of drug abuse.

But brain scans showed that both siblings had brains
unlike those of typical people, says Karen Ersche,
the study’s lead author.

“The fibers that connect the different parts of the
brain were less efficient in both,” she says.

These fibers connect areas involved in emotion with areas
that tell us when to stop doing something, Ersche says. When the fibers aren’t
working efficiently, she says, it takes longer for a “stop” message
to get through.

And sure enough, another experiment done by Ersche’s team
showed that both siblings took longer than a typical person to respond to a
signal telling them to stop performing a task. In other words, they had less
self-control.

That’s what you’d expect to find in addicts, Ersche says.

“We know that in people who are addicted to drugs
like cocaine, that self-control is completely impaired,” she says.
“These people use drugs and lose control on how much they use. They put
everything at risk, even their lives.”

But the fact that siblings without drug problems also had
impaired self-control offers strong evidence that these brain abnormalities are
inherited, Ersche says.

And she says the finding also raises a big question about
the siblings who aren’t addicts: “How do they manage with an abnormal
brain without taking drugs?”

Ersche hopes to conduct another study of the sibling
pairs that will answer that question.

In the meantime, the findings about self-control have
implications that go far beyond drug addiction, says Nora Volkow,
director of the National Institute on Drug Abuse.

“Self-control and the ability to regulate your
emotions really is an indispensable aspect of the function of the brain that
allows us to succeed,” she says.

That’s because the part of the brain that decides whether
to take a drug is also the part that helps us decide whether to speed through a
yellow light or drop out of school, she says.

And this brain circuit seems to be involved in a lot of
common disorders, she says.

“One of the ones that attracts the most attention is
ADHD [attention
deficit hyperactivity disorder], where kids are unable to control
their response to stimuli that distract them,” Volkow says.

Impulse control is also central to behaviors like
compulsive gambling and compulsive eating, she says.

The new study shows it’s possible to identify people who
have inherited a susceptibility to these sorts of problems, Volkow says. And it
should help researchers figure out how to help susceptible people strengthen
their self-control, she says.

“Predetermination is not predestination,”
Volkow says.

Source:

http://www.npr.org/blogs/health/2012/02/03/146307907/addicts-brains-may-be-wired-at-birth-for-less-self-control

In the first worldwide study of its kind, scientists from Toronto’s Centre for Addiction and Mental Health (CAMH) found evidence that heavy methamphetamine users might have a higher risk of developing schizophrenia. This finding was based on a large study comparing the risk among methamphetamine users not only to a group that did not use drugs, but also to heavy users of other drugs.

The report will be published online on Nov. 8, 2011, at AJP in Advance, the advance edition of the American Journal of Psychiatry, the official journal of the American Psychiatric Association.

Methamphetamine and other amphetamine-type stimulants are the second most common type of illicit drug used worldwide.

“We found that people hospitalized for methamphetamine dependence who did not have a diagnosis of schizophrenia or psychotic symptoms at the start of our study period had an approximately 1.5 to 3.0-fold risk of subsequently being diagnosed with schizophrenia, compared with groups of patients who used cocaine, alcohol or opioid drugs,” says Dr. Russ Callaghan, the CAMH scientist who led the study. Dr. Callaghan also found that the increased risk of schizophrenia in methamphetamine users was similar to that of heavy users of cannabis.

To establish this association, the researchers examined California hospital records of patients admitted between 1990 and 2000 with diagnosis of dependence or abuse for several major abused drugs: methamphetamine, cannabis, alcohol, cocaine or opioids. They also included a control group of patients with appendicitis and no drug use. The methamphetamine group had 42,412 cases, while cannabis had 23,335.

Records were excluded if patients were dependent on more than one drug or had a diagnosis of schizophrenia or drug-induced psychosis during their initial hospitalization. Readmission records within California hospitals were analyzed for up to 10 years after the initial admission. The researchers then identified patients who were readmitted with a schizophrenia diagnosis in each drug group.

There has been a longstanding debate as to whether there is a connection between methamphetamine use and schizophrenia. Many Japanese clinicians have long believed that methamphetamine might cause a schizophrenia-like illness, based on their observations of high rates of psychosis among methamphetamine users admitted to psychiatric hospitals. However, they lacked long-term follow-up studies of methamphetamine users initially free of psychosis. In North America, this link has mostly been discounted, as psychiatrists believed that the psychosis was already present and undiagnosed in these methamphetamine users.

“We really do not understand how these drugs might increase schizophrenia risk,” says Dr. Stephen Kish, senior scientist and head of CAMH’s Human Brain Laboratory. “Perhaps repeated use of methamphetamine and cannabis in some susceptible individuals can trigger latent schizophrenia by sensitizing the brain to dopamine, a brain chemical thought to be associated with psychosis.” Dr. Kish also cautions that the findings do not apply to patients who take much lower and controlled doses of amphetamines or cannabis for medical purposes.

Since this is the first such study showing this potential link, the researchers emphasize that the results need to be confirmed in additional research involving long-term follow-up studies of methamphetamine users.

“We hope that understanding the nature of the drug addiction-schizophrenia relationship will help in developing better therapies for both conditions,” says Dr. Callaghan.

In an earlier study using California hospital records, the researchers found evidence for a possible association between heavy methamphetamine use and Parkinson’s disease.

Source:www.eurekalert.org.  8th Nov. 2011

People with short-term drug-induced psychosis and longer-term mental illness, compounded by pot smoking, are seeking medical help at an increasing rate.   Mental Health Services clinical statewide director Peter Norrie said the Royal Hobart Hospital was seeing many cannabis cases.

First-time pot smokers were turning up at the Royal with full-blown psychosis — delusional, confused and anxious.   Other more regular pot smokers with long-term mental illness were fronting for treatment for episodes likely to have been triggered or related to using cannabis. 

“These days it’s close to every day,” said Dr Norrie, who is a senior clinical consultant psychiatrist at the Royal.   He said he was talking about “drug-induced psychosis or long-term mental illness associated with pot smoking”.   Dr Norrie said it was “very common” for first-time users to present with “floridly psychotic” behaviour.

He said psychiatrists were increasingly concerned with the link between substance abuse and mental illness.   Cannabis use had been linked with depression, anxiety and schizophrenia. International studies show modern strains of marijuana are from three to 10 times stronger than those used by previous generations.

“Clinically psychiatrists have suspected a link for many years and the latest research seems to confirm this,” Dr Norrie said.

“The chicken-and-egg debate has raged for years whether pot causes psychosis or people with a tendency to psychotic illness are predisposed to smoke pot.”

Dr Norrie said the first signs of schizophrenia were often a lack of engagement with society. But those symptoms could also be what is commonly known as “typically teenage” or a sign of the onset of depression.

Disengaged teenagers could then turn to cannabis.

If psychosis did occur it was hard to tell whether smoking pot was a cause or a symptom. Dr Norrie said some pot smokers appeared to be able to continue the habit without serious mental illness but others were prone to individual cases of psychosis or longer-term mental disease.

“There’s a certain group of people who smoke pot who are unlikely to develop mental illness but there’s certainly a significant number of the population who suffer from mental illness and pot smoking adds to the risk,” Dr Norrie said.

Drug-induced psychosis usually consists of paranoia, confusion and anxiety.

Sufferers present with memory problems and delusions. They can believe they have special powers, hear and see things that are not there and are unable to distinguish what is real.

Source: Sunday Tasmanian 30th January 2005

U.K. researchers measured the electrical activity from hundreds of neurons in the brains of rats given a drug that mimics the effects of cannabis, the psychoactive ingredient of marijuana.

The effects of the drug on individual brain regions were subtle but the drug completely disrupted the coordinated brain waves across the hippocampus and prefrontal cortex. Both of these brain structures are essential for memory and decision-making and play a key role in schizophrenia.

Due to the “decoupling” of the hippocampus and prefrontal cortex, the rats were unable to make accurate decisions while attempting to find their way through a maze, the University of Bristol researchers said.

“Marijuana abuse is common among sufferers of schizophrenia and recent studies have shown that the psychoactive ingredient of marijuana can induce some symptoms of schizophrenia in healthy volunteers. These findings are therefore important for our understanding of psychiatric diseases, which may arise as a consequence of ‘disorchestrated brains’ and could be treated by re-tuning brain activity,” lead author Matt Jones said in a university news release.

The study appears Oct. 25 in the Journal of Neuroscience.
“These results are an important step forward in our understanding of how rhythmic activity in the brain underlies thought processes in health and disease,” study first author Michal Kucewicz said

Source: www.everydayhealth.com Oct. 25, 2011

In the first worldwide study of its kind, scientists from Toronto’s Centre for Addiction and Mental Health (CAMH) found evidence that heavy methamphetamine users might have a higher risk of developing schizophrenia. This finding was based on a large study comparing the risk among methamphetamine users not only to a group that did not use drugs, but also to heavy users of other drugs.

 The report will be published online on Nov. 8, 2011, at AJP in Advance, the advance edition of the American Journal of Psychiatry, the official journal of the American Psychiatric Association.

Methamphetamine and other amphetamine-type stimulants are the second most common type of illicit drug used worldwide.

“We found that people hospitalized for methamphetamine dependence who did not have a diagnosis of schizophrenia or psychotic symptoms at the start of our study period had an approximately 1.5 to 3.0-fold risk of subsequently being diagnosed with schizophrenia, compared with groups of patients who used cocaine, alcohol or opioid drugs,” says Dr. Russ Callaghan, the CAMH scientist who led the study. Dr. Callaghan also found that the increased risk of schizophrenia in methamphetamine users was similar to that of heavy users of cannabis.

To establish this association, the researchers examined California hospital records of patients admitted between 1990 and 2000 with diagnosis of dependence or abuse for several major abused drugs: methamphetamine, cannabis, alcohol, cocaine or opioids. They also included a control group of patients with appendicitis and no drug use. The methamphetamine group had 42,412 cases, while cannabis had 23,335.

Records were excluded if patients were dependent on more than one drug or had a diagnosis of schizophrenia or drug-induced psychosis during their initial hospitalization. Readmission records within California hospitals were analyzed for up to 10 years after the initial admission. The researchers then identified patients who were readmitted with a schizophrenia diagnosis in each drug group.

There has been a longstanding debate as to whether there is a connection between methamphetamine use and schizophrenia. Many Japanese clinicians have long believed that methamphetamine might cause a schizophrenia-like illness, based on their observations of high rates of psychosis among methamphetamine users admitted to psychiatric hospitals. However, they lacked long-term follow-up studies of methamphetamine users initially free of psychosis. In North America, this link has mostly been discounted, as psychiatrists believed that the psychosis was already present and undiagnosed in these methamphetamine users.

“We really do not understand how these drugs might increase schizophrenia risk,” says Dr. Stephen Kish, senior scientist and head of CAMH’s Human Brain Laboratory. “Perhaps repeated use of methamphetamine and cannabis in some susceptible individuals can trigger latent schizophrenia by sensitizing the brain to dopamine, a brain chemical thought to be associated with psychosis.” Dr. Kish also cautions that the findings do not apply to patients who take much lower and controlled doses of amphetamines or cannabis for medical purposes.

Since this is the first such study showing this potential link, the researchers emphasize that the results need to be confirmed in additional research involving long-term follow-up studies of methamphetamine users.

“We hope that understanding the nature of the drug addiction-schizophrenia relationship will help in developing better therapies for both conditions,” says Dr. Callaghan.

In an earlier study using California hospital records, the researchers found evidence for a possible association between heavy methamphetamine use and Parkinson’s disease.

Source:www.eurekalert.org.  8th Nov. 2011

Correspondence:: kwelch1@staffmail.ed.ac.uk

Background
No longitudinal study has yet examined the association between substance use and brain volume changes in a population at high risk of schizophrenia.

Aims
To examine the effects of cannabis on longitudinal thalamus and amygdala-hippocampal complex volumes within a population at high risk of schizophrenia.

Method
Magnetic resonance imaging scans were obtained from individuals at high genetic risk of schizophrenia at the point of entry to the Edinburgh High-Risk Study (EHRS) and approximately 2 years later. Differential thalamic and amygdala-hippocampal complex volume change in high-risk individuals exposed (n = 25) and not exposed (n = 32) to cannabis in the intervening period was investigated using repeated-measures analysis of variance.

Results
Cannabis exposure was associated with bilateral thalamic volume loss. This effect was significant on the left (F = 4.47, P = 0.04) and highly significant on the right (F = 7.66, P = 0.008). These results remained significant when individuals using other illicit drugs were removed from the analysis.

Conclusions
These are the first longitudinal data to demonstrate an association between thalamic volume loss and exposure to cannabis in currently unaffected people at familial high risk of developing schizophrenia. This observation may be important in understanding the link between cannabis exposure and the subsequent development of schizophrenia.

 
Source:  bjp.rcpsych.org   Sept.2011

A common genetic profile that makes cannabis five times more likely to trigger schizophrenia and similar disorders has been identified, increasing pressure on the Government to reverse the drug’s reclassification from Class B to Class C.

The increased risk applies to people who inherit variants of a gene named COMT who also smoked cannabis as teenagers. About a quarter of the population have this genetic make-up, and up to 15 per cent of the group are likely to develop psychotic conditions if exposed to the drug early in life.

Neither the drug nor the gene raises the risk of psychosis by itself.

The study, led by Avshalom Caspi and Terrie Moffitt, of the Institute of Psychiatry at King’s College London, offers the best explanation yet for the way that cannabis has a devastating psychiatric impact on some users but leaves most unharmed. Scientists had suspected that genetic factors were responsible for this divide, but a gene had not been pinpointed.

The findings, to be published in Biological Psychiatry, also reinforce a growing consensus that nature and nurture are not mutually exclusive forces but combine to affect behaviour and health. The King’s team has previously identified genes that raise the risk of depression or aggression, but only in conjunction with environmental influences.

Mental health campaigners said that the results vindicated their concerns about the decision last year to downgrade cannabis to a Class C drug, which means that possession is no longer an arrestable offence.

Marjorie Wallace, chief executive of the mental health charity Sane, said that it was becoming clear that cannabis placed millions of users at risk of lasting mental illness. About fifteen million Britons have tried cannabis, and between two million and five million are regular users, according to the Home Office British Crime Survey. The research suggests that a quarter could be at risk.

The evidence will be considered by a review of the drug’s classification announced last month by the Home Secretary. It may be possible to develop a test for genetic susceptibility to cannabis. “If we were able genetically to identify the vulnerable individuals in advance, we would be able to save thousands of minds, if not lives,” Ms Wallace said.

Dr Caspi, however, rejected the idea of screening based on the COMT gene. “Such a test would be wrong more often than it is right. Cannabis has many other adverse effects, especially on developing teenagers, on respiratory health and possibly on cognitive function. Effects may be pronounced among a genetically vulnerable group but that doesn’t mean we should encourage others not genetically vulnerable to use cannabis.”

The King’s team tracked 803 men and women born in Dunedin, New Zealand, in 1972 and 1973, who were enrolled at birth in a research project. Each was interviewed at 13, 15 and 18 about cannabis use, tested to determine which type of COMT genes they had inherited, and followed up at 26 for signs of mental illness.

COMT was chosen as it is known to play a part in the production of dopamine, a brain-signalling chemical that is abnormal in schizophrenia. It comes in two variants, known as valine or methionine, and every person has two copies, one from each parent.

Among people with two methionine variants, the rate of psychotic illness was 3 per cent, the background rate for the general population, regardless of whether they had used cannabis as teenagers.

Among those with two valine variants the rate was 3 per cent for non-users but 15 per cent for those who had smoked cannabis in their teens.

Dr Caspi said research had shown that the valine gene variant and cannabis affect the brain’s dopamine system in similar fashion, suggesting that they deliver a “double dose” that can be damaging. The work needs to be replicated by others to confirm the findings, Dr Caspi said. It also is possible that the gene involved is not COMT but a neighbour.

THE DRUG OF CHOICE FOR MILLIONS

• Cannabis was reclassified from a Class B to a Class C drug in January 2004. Possession remains illegal, but is not an arrestable offence. The Home Secretary has asked for a review by November
• The Home Office estimates that fifteen million people have tried cannabis, two million to five million are regular users and reclassification has saved 199,000 hours’ police work
• Liberalisation campaigners argue that millions smoke the drug with fewer ill-effects than others suffer from alcohol or tobacco
• A recent study at Maastricht University found that cannabis doubles the risk of schizophrenia, hallucinations and paranoia among a genetically susceptible group

Source: www.timesonline.co.uk 14 April 2005

Source: The Independent. 26th October 2011

*Nicotine, aspirin, alcohol, and drugs administered after the crash are excluded. Testing positive for drugs only means that the drugs were found in the driver’s system and does not imply impairment or indicate that drug use was the cause of the crash or the fatality.

SOURCE: Adapted by CESAR from National Highway Traffic Safety Administration (NHTSA),
drug Involvement of Fatally Injured Drivers,” Traffic Safety Facts, November 2010.
Available online at http://www-nrd.nhtsa.dot.gov/Pubs/811415.pdf

From the Molecular Neuropsychiatry Branch, National Institute on Drug Abuse, National Institutes of Health,Baltimore,MD.

Address correspondence and reprint requests to Dr. Ronald I. Herning, Molecular Neuropsychiatry Branch, National Institute on Drug Abuse, PO Box 5180, Baltimore, MD21224; e-mail: rherning@intra.nida.nih.gov

Objective: To determine possible effects of prolonged marijuanause on the cerebrovascular system during a month of monitoredabstinence and to assess how the intensity of current use mighthave influenced cerebrovascular perfusion in these marijuanausers.

Method: The authors recorded blood flow velocity in the anteriorand middle cerebral arteries using transcranial Doppler sonographyin three groups of marijuana users who differed in the intensityof recent use (light: n = 11; moderate: n = 23; and heavy: n= 20) and in control subjects (n = 18) to assess the natureand duration of any potential abnormalities. Blood flow velocitywas recorded within 3 days of admission and 28 to 30 days ofmonitored abstinence on an inpatient research unit in orderto evaluate subacute effects of the drug and any abstinence-generatedchanges.

Results: Pulsatility index, a measure of cerebrovascular resistance,and systolic velocity were significantly increased in the marijuanausers vs control subjects. These increases persisted in theheavy marijuana users after a month of monitored abstinence.

Conclusions: Chronic marijuana use is associated with increasedcerebrovascular resistance through changes mediated, in part,in blood vessels or in the brain parenchyma. These findingsmight provide a partial explanation for the cognitive deficitsobserved in a similar group of marijuana users.

Source:  NEUROLOGY 2005;64:488-493

The meta-analysis found that people who smoked marijuana developed psychotic disorders an average 2.7 years earlier than people who did not use cannabis
Context  A number of studies have found that the use of cannabis and other psychoactive substances is associated with an earlier onset of psychotic illness.
Objective  To establish the extent to which use of cannabis, alcohol, and other psychoactive substances affects the age at onset of psychosis by meta-analysis.
Data Sources  Peer-reviewed publications in English reporting age at onset of psychotic illness in substance-using and non–substance-using groups were located using searches of CINAHL, EMBASE, MEDLINE, PsycINFO, and ISI Web of Science.
Study Selection  Studies in English comparing the age at onset of psychosis in cohorts of patients who use substances with age at onset of psychosis in non–substance-using patients. The searches yielded 443 articles, from which 83 studies met the inclusion criteria.
Data Extraction  Information on study design, study population, and effect size were extracted independently by 2 of us.
Data Synthesis  Meta-analysis found that the age at onset of psychosis for cannabis users was 2.70 years younger (standardized mean difference = –0.414) than for nonusers; for those with broadly defined substance use, the age at onset of psychosis was 2.00 years younger (standardized mean difference = –0.315) than for nonusers. Alcohol use was not associated with a significantly earlier age at onset of psychosis. Differences in the proportion of cannabis users in the substance-using group made a significant contribution to the heterogeneity in the effect sizes between studies, confirming an association between cannabis use and earlier mean age at onset of psychotic illness.
Conclusions  The results of meta-analysis provide evidence for a relationship between cannabis use and earlier onset of psychotic illness, and they support the hypothesis that cannabis use plays a causal role in the development of psychosis in some patients. The results suggest the need for renewed warnings about the potentially harmful effects of cannabis.
Matthew Large, BSc(Med), MBBS, FRANZCP; Swapnil Sharma, MBBS, FRANZCP; Michael T. Compton, MD, MPH; Tim Slade, PhD; Olav Nielssen, MBBS, MCrim, FRANZCP
Source: Arch Gen Psychiatry. Published online February 7, 2011. doi:10.1001/archgenpsychiatry.2011.5

Delta (9)-tetrahydrocannabinol (THC), the most important psychoactive substance in cannabis, is frequently detected in blood from apprehended drivers suspected for drugged driving. Both experimental and epidemiological studies have demonstrated the negative effects of THC upon cognitive functions and psychomotor skills. These effects could last longer than a measurable concentration of THC in blood. Culpability studies have recently demonstrated an increased risk of becoming responsible in fatal or injurious traffic accidents, even with low blood concentrations of THC. It has also been demonstrated that there is a correlation between the degree of impairment, the drug dose and the THC blood concentration. It is very important to focus on the negative effect of cannabis on fitness to drive in order to prevent injuries and loss of human life and to avoid large economic consequences to the society.

 Source:  Tidsskr Nor Laegeforen. 2007 Mar 1;127(5):583-4.

Researchers at the University of California, Los Angeles, found that some of the brain regions of meth-exposed children were even smaller than in alcohol-exposed children. One such region is the caudate nucleus, which plays a role in learning, memory, motor control, and motivation.

“Our findings stress the importance of drug abuse treatment for pregnant women,” said research team leader Elizabeth Sowell.

According to Sowell and her colleagues, being able to identify which brain structures are affected in meth-exposed children may help predict the specific types of leaning and behavioral problems that will afflict these children.

 Source:  The Journal of Neuroscience. March 17 2011

In a report in The Herald newspaper today, researchers at theUniversity of Cambridge have identified the abnormalities in the frontal lobe of cocaine users’ brains which are linked to their compulsive cocaine-using behaviour. Scientists think these abnormalities could help explain why some people are more prone to drug dependency.

The researchers, led by Dr Karen Ersche of the University’s Behavioural and Clinical Neuroscience Institute,  scanned the brains of 120 people, half of whom had a dependence on cocaine.   They found that the cocaine users had widespread loss of grey matter which was directly related to the duration of their cocaine use and that this reduction in volume was associated with greater compulsivity to take cocaine.

The scientists also found that parts of the brain reward system where cocaine exerts its actions were significantly enlarged in cocaine users. This was not linked to the duration of the user’s habit.

The researchers believe this may suggest that alterations in the brain’s reward system predate cocaine use, possibly making these individuals more vulnerable to the effects of the drug.

The Advisory Council on the Misuse of Drugs is currently carrying out a review of the harms associated with cocaine.

Source:  www.heraldscotland.com  11^th June 2011

Young women’s brains are particularly vulnerable to harm from alcohol because they develop earlier than men’s.  Tests on 95 adolescents aged 16 to 19 were carried out by researchers at severalUSuniversities.

The study is published in Alcoholism: Clinical & Experimental Research.

Researchers recruited 27 binge-drinking males and 13 females and gave them neurophsychological tests and “spatial working memory” tests to complete.

Binge-drinking young women were defined as those drinking more than three pints of beer or more than four glasses of wine at one sitting. Binge-drinking men drank four pints of beer or a bottle of wine.   The same tests were then carried out on 31 males and 24 females who did not have episodes of drinking heavily and the results compared.

Using MRI scans, the study team found that female teenage heavy drinkers had less brain activation in several brain regions than female non-drinking teens when doing the same spatial task.  They suggested that this could cause problems when driving, playing sports involving complex moves, using a map or remembering how to get somewhere.

Susan Tapert, professor of psychiatry at theUniversityofCaliforniaand lead study author, said these differences in brain activity negatively affected other functions, like concentration and “working memory”.

The study describes “working memory” as using and working with information that is in your mind, like adding up numbers. It is also critical to logical thinking and reasoning.  But the young men studied were not affected to the same extent, Dr Tapert said.   “Male binge drinkers showed some, but less, abnormality as compared to male non-drinkers. This suggests that female teens may be particularly vulnerable to the negative effects of heavy alcohol use.”

Fluctuations

Previous research has shown that among adult alcoholics, women are more vulnerable to the damaging effects of alcohol on the brain than men.

Edith Sullivan, a professor in psychiatry and behavioural sciences atStanfordUniversity, said that the brains of adolescent boys and girls appear to be affected differently by alcohol.  “Females’ brains develop one to two years earlier than males, so alcohol use during a different developmental stage – despite the same age – could account for the gender differences.

“Hormonal levels and alcohol-induced fluctuations in hormones could also account for the gender differences. Finally, the same amount of alcohol could more negatively affect females since females tend to have slower rates of metabolism, higher body fat ratios, and lower body weight.”

Don Shenker, from Alcohol Concern, said the research demonstrates why reducing binge drinking among young people must be an urgent priority. “Ministers should go much further to clamp down on off-licence promotions which are driving under-age drinking and reviewing the extent of alcohol marketing which young people are exposed to and which makes drinking appear attractive.

“We have to also look at intervening as early as possible so that when teenagers go to A&E as a result of drinking or in trouble with the police or at school, they are provided with the right advice and support to reduce their risky drinking and make healthier choices.”

A Department of Health spokeswoman said “We are already taking action to tackle problem drinking, including plans to stop supermarkets selling below cost alcohol and working to introduce a tougher licensing regime.   ”Our recent white paper set out our plan to ring-fence public health spending and give power to local communities to improve the health of local people and this includes improving alcohol treatment services through a greater focus on outcomes and payment by results.   We will also be publishing a new alcohol strategy later this year to follow on from the public health white paper.”

Source: www.bbc.co.uk  16^th July 2011

OBJECTIVE:

Prenatal cocaine exposure has been associated with alterations in neonatal behavior and more recently a dose-response relationship has been identified. However, few data are available to address the long-term behavioral effects of prenatal exposures in humans. The specific aim of this report is to evaluate the school-age behavior of children prenatally exposed to cocaine.

METHODS:

All black non-human immunodeficiency virus-positive participants in a larger pregnancy outcomes study who delivered singleton live born infants between September 1, 1989 and August 31, 1991 were eligible for study participation. Staff members of the larger study extensively screened study participants during pregnancy for cocaine, alcohol, cigarettes, and other illicit drugs. Prenatal drug exposure was defined by maternal history elicited by structured interviews with maternal and infant drug testing as clinically indicated. Cocaine exposure was considered positive if either history or laboratory results were positive. Six years later, 665 families were contacted; 94% agreed to participate. The child, primary caretaker (parent), and, when available, the biologic mothers were tested in our research facilities. Permission was elicited to obtain blinded teacher assessments of child behavior with the Achenbach Teacher’s Report Form (TRF). Drug use since the child’s birth was assessed by trained researchers using a structured interview.

RESULTS:

Complete laboratory and teacher data were available for 499 parent-child dyads, with a final sample size for all analyses of 471 (201 cocaine-exposed) after the elimination of mentally retarded subjects. A comparison of relative Externalizing (Aggressive, Delinquent) to Internalizing (Anxious/Depressed, Withdrawn, Somatic Complaints) behaviors of the offspring was computed for the TRF by taking the difference between the 2 subscales to create an Externalizing-Internalizing Difference (T. M. Achenbach, personal communication, 1998). Univariate comparisons revealed that boys were significantly more likely to score in the clinically significant range on total TRF, Externalizing-Internalizing, and Aggressive Behaviors than were girls. Children prenatally exposed to cocaine had higher Externalizing-Internalizing Differences compared with controls but did not have significantly higher scores on any of the other TRF variables. Additionally, boys prenatally exposed to cocaine were twice as likely as controls to have clinically significant scores for externalizing (25% vs 13%) and delinquent behavior (22% vs 11%). Gender, prenatal exposures (cocaine and alcohol), and postnatal risk factors (custody changes, current drug use in the home, child’s report of violence exposure) were all related to problem behaviors. Even after controlling for gender, other prenatal substance exposures, and home environment variables, cocaine-exposed children had higher Externalizing-Internalizing Difference scores. Prenatal exposure to alcohol was associated with higher total score, increased attention problems, and more delinquent behaviors. Prenatal exposure to cigarettes was not significantly related to the total TRF score or any of the TRF subscales. Postnatal factors associated with problem behaviors included both changes in custody status and current drug use in the home. Change in custody status of the cocaine-exposed children, but not of the controls, was related to higher total scores on the TRF and more externalizing and aggressive behaviors. Current drug use in the home was associated with higher scores on the externalizing and aggressive subscales.

CONCLUSIONS:

Results of this study suggest gender-specific behavioral effects related to prenatal cocaine exposure. Prenatal alcohol exposure also had a significant impact on the TRF. Postnatal exposures, including current drug use in the home and the child’s report of violence exposure, had an independent effect on teacher-assessed child behavioral problems.

Source:  Pediatrics. 2000 Oct;106(4):782-91.

The synthetic cannabinoid (cannabis-related) compound, called MDA19, seems to avoid side effects by acting mainly on one specific subtype of the cannabinoid receptor. “MDA19 has the potential for alleviating neuropathic pain without producing adverse effects in the central nervous system,” according to the study by Dr Mohamed Naguib of The University of Texas M.D. Anderson Cancer Center.

MDA19 Works on a Single Cannabinoid Receptor
The researchers performed a series of experiments to analyze the pharmacology and effects of the synthetic cannabinoid MDA19. There are two subtypes of the cannabinoid chemical receptor: CB1, found mainly in the brain; and CB2, found mainly in the peripheral immune system.

Dr. Naguib’s group has been doing research to see if the cannabinoid receptors—particularly CB2—can be a useful target for new drugs to treat neuropathic pain. Neuropathic pain is a difficult-to-treat type of pain caused by nerve damage, common in patients with trauma, diabetes, and other conditions.

MDA19 was designed to have a much stronger effect on the CB2 receptor than on the CB1 receptor. In humans, MDA19 showed four times greater activity on the CB2 receptor than on the CB1 receptor. In rats, the difference was even greater. The experiments also showed that MDA19 had “protean” effects, so-called after the shape-shifting Greek sea god Proteus—under different conditions, it could either block or activate the cannabinoid receptors.

In rats, treatment with MDA19 effectively reduced specific types of neuropathic pain, with greater effects at higher doses. At the same time, it did not seem to cause any of the behavioral effects associated with marijuana.

Potential to Develop Effective Pain Drugs that Avoid Side Effects
The “functional selectivity” of MDA19—the fact that it acts mainly on the CB2 receptor and has a range of effects under differing conditions—could have important implications for drug development. “[W]ith functionally selective drugs, it would be possible to separate the desired from the undesired effects of a single molecule through a single receptor,” Dr. Naguib and colleagues write.
This means that MDA19 could be a promising step toward developing medications that have the pain-reducing effect of cannabinoids while avoiding the mental and physical side effects of marijuana itself. However, more research will be needed before MDA19 or other agents that act on the CB2 receptor are ready for testing in humans.

“These elegant studies by Professor Naguib demonstrate remarkable analgesic properties for this synthetic cannabinoid,” comments Dr. Steven L. Shafer of Columbia University, Editor-in-Chief of Anesthesia &Analgesia. “The studies suggest a novel mechanism for this protean agonist. Although preliminary, these studies suggest that synthetic cannabinoids may be significant step forward for patients suffering from neuropathic pain.”

SOURCE : www.news-medical.net 2nd July 2010

This study is the first demonstration that a correlation exists between synaptic plasticity and the transition to addiction. The results from the teams at Neurocentre Magendie call into question the hitherto held idea that addiction results from pathological cerebral modifications, which develop gradually with drug usage.

Their results show that addiction may, instead, come from a form of anaplasticity, i.e. from incapacity of addicted individuals to counteract the pathological modifications caused by the drug to all users.

The voluntary consumption of drugs is a behaviour found in many species of animals. However, it had long been considered that addiction, defined as compulsive and pathological drug consumption, is behaviour specific to the human species and its social structure.

In 2004, the team of Pier Vincenzo Piazza showed that the behaviours which define addiction in humans, also appear in some rats which will self administer cocaine. Addiction exhibits astonishing similarities in men and rodents, in particular the fact that only a small number of consumers (humans or rodents) develop a drug addiction. The study of drug dependent behaviour in this mammal model thus opened the way to the study of the biology of addiction.

Today, thanks to a fruitful collaboration, the teams of Pier Vincenzo Piazza and Olivier Manzoni are reporting discovery of the first known biological mechanisms for the transition from regular but controlled drug taking to a genuine addiction to cocaine, characterised by a loss of control over drug consumption.

Chronic exposure to drugs causes many modifications to the physiology of the brain. And researchers wanted to find out which of these modifications is responsible for the development of an addiction.
The addiction model developed in Bordeaux provides a unique tool to answer this question. Thus it allows comparing animals who took identical quantities of drugs, but of which only few become addicted.

By comparing addict and non-addict animals at various time points during their history of drug taking, the teams of Pier Vincenzo Piazza and Olivier Manzoni have demonstrated that the animals which developed an addiction to cocaine exhibit a permanent loss of the capacity to produce a form of plasticity known as long-term depression (or LTD).

LTD refers to the ability of the synapses (the region of communication between neurons) to reduce their activity under the effect of certain stimulations. It plays a major role in the ability to develop new memory traces and, consequently, to demonstrate flexible behaviour.

After short-term usage of cocaine, LTD is not modified. However, after a longer use, a significant LTD deficit appears in all users. Without this form of plasticity, which allows new learning to occur, behaviour with regard to the drug becomes more and more rigid, opening the door to development of a compulsive consumption.

The brain of the majority of users is able to produce the biological adaptations which allow to counteract the effects of the drug and to recover a normal LTD.
By contrast, the anaplasticity (or lack of plasticity) exhibited by the addicts leaves them without defences and hence the LTD deficit provoked by the drug becomes chronic.

This permanent absence of synaptic plasticity would explain why drug seeking behaviour becomes resistant to environmental constraints (difficulty in procuring the substance, adverse consequences of taking the drug on health, social life, etc.) and consequently more and more compulsive. Gradually, control of the taking of the drug is lost and addiction appears.

For Pier-Vincenzo Piazza and his collaborators, these discoveries also have important implications for developing new treatment of addiction.

“We are probably not going to find new therapies by trying to understand the modifications caused by a drug in the brains of drug addicts,” explain the researchers, “since their brain is anaplastic.” For the authors, “The results of this work show that it is in the brain of the non-addicted users that we will probably find the key to a true addiction therapy.

Indeed,” the authors estimate, “understanding the biological mechanisms which enable adaptation to the drug and which help the user to maintain a controlled consumption could provide us with the tools to combat the anaplastic state that leads to addiction”. (ANI)

Source: www.sify.com/news 2010-06-29

In the study, researchers at The Scripps Research Institute in Jupiter, Florida found that cocaine consumption increased levels of a specific microRNA sequence in the brains of rats, named microRNA-212.

As its levels increased, the rats exhibited a growing dislike for cocaine, ultimately controlling how much they consumed.
On the other hand, as levels of microRNA-212 decreased, the rats consumed more cocaine and became the rat equivalent of compulsive users.

The study’s findings suggest that microRNA-212 plays a pivotal role in regulating cocaine intake in rats and perhaps in vulnerability to addiction.
Interestingly, the same microRNA-212 identified in this study, is also expressed in the human’s dorsal striatum, a brain region that has been linked to drug abuse and habit formation.

“This study enhances our understanding of how brain mechanisms, at their most fundamental levels, may contribute to cocaine addiction vulnerability or resistance to it,” Nature quoted National Institute on Drug Abuse (NIDA) Director Dr. Nora D. Volkow, as saying.

“This research provides a wonderful example of how basic science discoveries are critical to the development of new medical treatments and targeted prevention,” he added.

Rats with a history of extended cocaine access can demonstrate behavior similar to that observed in humans who are dependent on the drug.
Current data show that about 15 percent of people who use cocaine become addicted to it.
The findings suggest that microRNAs may be important factors
contributing to this vulnerability.

“The results of this study offer promise for the development of a totally new class of anti-addiction medications. Because we are beginning to map out how this specific microRNA works, we may be able to develop new compounds to manipulate the levels of microRNA-212 therapeutically with exquisite specificity, opening the possibility of new treatments for drug addiction,” said Paul J. Kenny, senior author on the study.
The study is published in the journal Nature. (ANI)

Source:www.sify.com/news 9th July 2010-07-10

Marijuana use alters perceptions and creates time distortion and can cause drowsiness and lethargy. Heavy marijuana use can cause apathy, decreased motivation, and impair cognitive performance and can cause mental health problems.

Employees who use marijuana off-duty are still effected by it. Impaired cognition that can cause lapses in judgement can remain for a long period. Memory defects can last as long as six weeks. See: Abbie Crites-Leoni, Medicinal Use of Marijuana: Is the Debate a Smoke Screen for Movement Toward Legalization? 19 J. Legal Med. 273, 280 (1998) (citing Schwartz, et al., Short- Term Memory Impairment in Cannabis-Dependent Adolescents, 143 Am. J. Dis. Child. 1214 (1989)

Employers may be liable for the actions of employee who use marijuana especially those employees in safety sensitive positions. The more chronic the use of “medical” marijuana the higher the risk.

VIOLATIONS OF FEDERAL LAW

Will employers have to accommodate marijuana use that violates federal law? Marijuana, remains illegal under federal law because of its “high potential for abuse,” its lack of any “currently accepted medical use in treatment in the United States,” and its “lack of accepted safety for use … under medical supervision.”Gonzales v. Raich, 545 U.S. 1 (2005); United States v. Oakland Cannabis Buyers’ Cooperative, 532 U.S. 483 (2001)

IF THIS BILL PASSES “MEDICAL” MARIJUANA WILL RESULT IN MORE MARIJUANA USE AMONG EMPLOYEES

As consumers we all pay for lost productivity and job-related accidents in the final costs of the produced goods and higher insurance premiums due to workplace accidents. Drug using employees are not as safe. They are 3.6 times more likely to be involved in a work-related accident than their non-using employee, and 5 times more likely to file workers’ compensation claims. As many as 50% of all workers’ compensation claims may involve substance abuse.[FN1]

The U.S. Postal Service did a study that showed that substance abusers have 55% more accidents, experience 85% more on-the-job injuries, and have a 78% higher rate of absenteeism when compared to non-substance abusing employees.[FN2] A report by the National Safety Council claimed that 80% of those injured in serious drug-related work accidents are not the drug using employees, but innocent employees and others.[FN3]

Drug using employees commit workplace crimes. There is a very significant statistical correlation between drug use and criminal conduct.[FN4]

Substance abuse also causes:
Domestic and financial difficulties for employees;
Poor judgment in employment decision making;
Potential embarrassment to the employer as a result of off-duty conduct, which may be publicized, including criminal charges, diversion of supervisory and managerial time;
Damage to company property; and
Time devoted to discipline and grievance matters.[FN5]

While the studies vary somewhat, it is clear that there is substantial substance abuse in the workplace and it has a powerful negative impact on our economy and productivity. The increased use of “medical” marijuana will magnify all these problems.

References

[FN1] Current, The Truth About Drug Testing: Answers to the Questions Everyone Is Asking, p. 3 (1st Ed., Fort Lauderdale, FL, 1998).

[FN2] “Pre-employment Drug Testing: Association with EAP, Disciplinary, and Medical Claims Information” U.S. Postal Service, Personnel Research and Development Branch, Office of Selection and Evaluation, July 1992.

[FN3] Wisotsky, The Ideology of Drug Testing [Ideology of Drug Testing], 11 Nova L Rev 763, 768 (1987).

[FN4] See Stewart, Proof Positive of Drug Link to Crime, Wall St J, May 28, 1987, at 26, col 3.

[FN5]Alcohol & Drugs in the Workplace: Costs, Control and Controversies, A BNA Special Report [Costs, Control and Controversies], 7 (Bureau of National Affairs, Washington, D.C. 1986)

Source: David Evans sent to DFAF May 2010

The study, published online in the American Journal of Public Health, found that a 10 percent increase in cigarette pricing resulted in an 18.2 percent decline in smoking among people in these groups.

The findings demonstrate that increasing cigarette taxes could be a way to curb smoking, which is still the leading preventable cause of death in the United States, according to the study’s lead author, Dr. Michael Ong, an assistant professor of medicine in the division of general internal medicine and health services research at the Geffen School of Medicine.
“Whatever we can do to reduce smoking is critical to the health of the U.S.,” said Ong, who is also a researcher at UCLA’s Jonsson Cancer Center. “Cigarette taxes are used as a key policy instrument to get people to quit smoking, so understanding whether people will really quit is important.

Individuals with alcohol, drug or mental disorders comprise 40 percent of remaining smokers, and there is little literature on how to help these people quit smoking.”

Prior research on the effect of cigarette pricing on smoking, which had been conducted using information from 1991, suggested that individuals with mental illness were less likely than other individuals to quit due to price increases. Unlike that research, however, the current study expanded the research to include people with alcohol and drug disorders.

The researchers based their work on data from 7,530 individuals from the 2000-01 Healthcare for Communities Household Survey. Of those, 2,106 people, or 23 percent, had alcohol, drug or mental disorders during the previous year. Of that group, 43.8 percent were smokers — a much higher proportion than among rest of the population.

Though the researchers found that people with alcohol dependence did not cut down on cigarettes when prices rose, people with binge-drinking problems, substance-use disorders and mental disorders were significantly more likely to quit smoking if prices rose, as would occur with a cigarette tax increase.

While the study does suggest that increasing cigarette prices through taxation could reduce smoking among individuals with alcohol, drug or mental disorders, the authors note that further study is needed to determine if recent cigarette price increases have reduced smoking among individuals with such disorders, and whether the identified association is causal.

Source: http://www.sciencedaily.com/releases June 3, 2010

The drug works by blocking the right amount of the feel good effects of alcohol (brought on by increased levels of dopamine), making drinking less enjoyable and thus reducing cravings and helping to stop heavy drinking.

Topiramate was also found to lower blood pressure and cholesterol levels which may lead to a decrease in heart disease in alcohol dependent patients.

Alcoholism affects over 17 million people. Without proper treatment, it’s a devastating disease that can ruin lives and relationships. A new therapy that comes in a pill is bringing new hope to alcoholics.

There was a time in Christine Flemming’s life when alcohol came before her kids.
“I can’t remember when my daughter was very little, because I was drinking so much,” said Flemming. “That affected me a lot.”

Flemming needed help, but traditional treatment methods didn’t work. Now she’s on a new kind of therapy in the form of a pill called topiramate. It has changed her life. “I can tell you that it cuts my cravings, and I don’t feel like I have to drink,” Flemming said. “I don’t feel like that’s something I need in my life and I have to do.”

Alcohol increases levels of dopamine, a chemical in the brain that makes us feel good. The drug works by blocking the right amount of the feel-good effects from alcohol to reduce cravings and help stop heavy drinking. During clinical trials, neuropharmacologists were surprised to learn it also lowers blood pressure and cholesterol levels, which may lead to a decrease in heart disease in alcohol dependent patients.

“Most of the morbidity due to alcoholism is caused by secondary effects of all these other systems, so to have a drug that begins to correct all those other physical abnormalities is extremely helpful,” said Bankhole Johnson, Ph.D., a Neuropharmacologist at the University of Virginia in Charlottesville, Va.

The drug helped improve Fleming’s health and end her dependence on alcohol. She cut her drinking from 15 beers a day to just three, so time with her kids is now a priority.
“It’s made a big difference,” Flemming said. “It’s made a really big difference, and I feel like I’m actually there for my family.”

Qualifying patients can find out how to receive the drug by contacting their primary care doctors.

WHAT IS TOPIRAMATE? Topiramate is a drug originally discovered in 1979. It is prescribed as an epilepsy medication and for migraine headaches. It is also used for a number of other purposes, including as a treatment for people with alcoholism.

Researchers believe that topiramate works in two ways. First, it reduces the release of dopamine that follows the consumption of alcohol. This reduces the positive feeling that people receive from alcohol, and thus reduce the incentive to drink. Second, topiramate interferes with the protein glutamate which normally excites dopamine neurons and again, lessening the ýfeel goodý effect of dopamine from alcohol.

WHAT IS ALCOHOL? Alcohol is created through the natural process of fermentation. This happens when yeast and sugar from vegetables and grains change the sugar into alcohol. When you drink alcohol, it is absorbed into your bloodstream, where it can affect the central nervous system, which is the control center for your entire body.

Alcohol slows down this control center with its sedative effect. In moderation it can reduce anxiety, but it also blocks some of the commands the brain sends to other parts of the body, so it alters your senses. That’s why, when drunk, people often have trouble walking, talking, and some may even “black out,” forgetting what they said or did. Drinking an excessive amount of alcohol can even be fatal.

Source www.ScienceDaily June 2010

Ecstasy (MDMA) is a stimulant drug widely used recreationally that is also being tested in clinical trials for the treatment of post-traumatic stress disorder.
Led by Dr. Stephen Kish at CAMH, this study provides confirmation of a previous finding from Johns Hopkins University that levels of the serotonin transporter (SERT) are low in cerebral cortex of chronic ecstasy users. The subjects were “typical” ecstasy users who used about two tablets of the drug twice a month.

SERT is a protein responsible for regulating levels of serotonin, a neurotransmitter important for mood and impulse control. Ecstasy interacts with SERT to cause the release of serotonin, an action that probably explains some of the behavioral effects of the drug such as increased sociability.

Scientists have long suspected that ecstasy might harm brain cells that use serotonin, but 12 years of brain scan studies have produced contradictory results, even within the same laboratory.
The CAMH study used a large subject size (49 drug users, 50 control subjects), confirmed by hair analysis that ecstasy users actually used the drug, and used an imaging probe that could measure SERT throughout the brain.
“We were surprised to discover that SERT was decreased only in the cerebral cortex and not throughout the brain, perhaps because serotonin nerves to the cortex are longer and more susceptible to changes. This finding is almost identical to newer data from Johns Hopkins and is the first time that one laboratory has actually been able to replicate results of another independent laboratory in a SERT study of ecstasy users.” said Dr. Kish.

Drug hair analysis indicated that many ecstasy users, probably unknowingly, also used methamphetamine, which might itself damage serotonin cells; however, low SERT was found both in ecstasy users who used and who did not use methamphetamine. Dr. Jason Lerch at SickKids showed that those ecstasy users who also used methamphetamine had a slightly thinner cerebral cortex.

Does low SERT equal “structural brain damage”? “Not necessarily” said co-author Dr. Isabelle Boileau of CAMH. “There is no way to prove whether low SERT is explained by physical loss of the entire serotonin nerve cell, or by a loss of SERT protein within an intact nerve cell.”
Dr. Kish suggests that low SERT might explain why many ecstasy users need to keep increasing the dose to experience the same effects, since SERT is necessary for the action of ecstasy. “Most of the ecstasy users of our study complained that the first dose is always the best, but then the effects begin to decline and higher doses are needed. The need for higher doses, possibly caused by low SERT, could well increase the risk of harm caused by this stimulant drug,” said Dr. Kish.

Media Contact: Michael Torres, Media Relations, CAMH ; 416 595 6015 or email media@camh.net

Source: www.camh.net 18th May 2010

The study was a ‘real-world’ test of a promising Dutch internet-based self-help intervention for problem drinking.
A previous randomised trial employing the methodological safeguards possible in tightly controlled research (particularly the recruitment of a comparison group not given access to the intervention) had established that the intervention reduced drinking. At issue in the featured study was whether similar drinking reductions would be seen when the intervention was made freely available to the general public. If they were, then the assumption could be made that these too were caused by having access to the intervention.

Drinking Less is an on-line, interactive programme with no personal therapist input. Aimed at risky drinkers among the general adult population, the intervention is based on principles derived from motivational interviewing, cognitive-behavioural therapies and self-control training. Its home page offers links to alcohol-related information, treatment services, a discussion forum, and the

Drinking Less self-help programme, the core of the intervention. Over a recommended six weeks (though this is entirely up to the user) the programme guides visitors in preparing to change their drinking, setting goals , implementing change, and finally sustaining it, preferably by drinking within recommended limits.

The earlier trial had found that six months later, at least 17% of adult problem drinkers randomly allocated to this intervention had reduced their drinking to within Dutch guidelines, compared to just 5% allocated to an on-line alcohol education brochure. Before the study, both groups had averaged about 55 UK units a week.

At follow-up, the Drinking Less group had cut consumption to about 36 UK units a week, but the brochure group had barely changed.

The featured study monitored what happened when over 10 months spanning 2007 and 2008 the web site was advertised to the Dutch public. During this time round 27,500 people visited the site, of whom 1625 signed up for the self-help programme, accessing it on average 23 times.

Typically they were well educated, employed, middle-aged men. On average they drank about 50 UK units a week, and nearly all who completed the on-line AUDIT screening questionnaire scored in a range indicative of alcohol abuse or dependence.
During the first seven of the 10 months, 378 of site visitors who signed up to the Drinking Less programme also agreed to participate in research to assess its impact. On average they drank roughly the same amount (95% exceeded Dutch guidelines) as all 1625 who signed up and were also similar in age, sex, employment, and motivation to change.

Despite some statistically significant differences, they were also broadly similar to participants in the earlier randomised trial. Over 8 in 10 had never received professional help for their drinking. A few weeks later a survey suggested that after signing up, nearly 9 in 10 went on to use the programme, though generally only a few times.
Of the 378 in the baseline sample, 153 responded to an on-line follow-up survey six months later. Before signing up to the programme, just 4% had confined their drinking within Dutch guidelines; six month later, 39% did so. They had also nearly halved their average consumption from 50 UK units to 27. On the ‘fail-safe’ assumption that the intervention had no impact on people who were not followed up, still the drinking reductions were statistically significant; from 5%, the proportion drinking within guidelines rose to 19%, and consumption fell from 51 UK units to 42.

Next the analysts compared these results with those from the six-month follow-up in the randomised trial. Based only on respondents to the follow-up surveys, and adjusting for differences between the samples, in the ‘real-world’ test over twice as many (unadjusted figures 36% v. 19%) people moved to drinking within Dutch guidelines. When the assumption was made that in both trials the intervention had no impact on people not followed up, the figures still favoured the ‘real-world’ test (15% v. 10%), but the difference was no longer statistically significant.

The researchers concluded that the featured study had shown that the benefits established by the randomised controlled trial would be sustained when the intervention was made routinely and generally available to the public. The expected throughput of 3000 Drinking Less programme users a year would amount to nearly 3% of the country’s problem drinkers who would otherwise not have received professional help. Probably because they require the drinker to take the initiative and visit the site, such interventions reach people who, compared to the totality of problem drinkers, are more likely to be women, employed, highly educated, and motivated to change their drinking. Given its low cost per user, this type of intervention seems to have a worthwhile place in a public health approach to reducing alcohol-related problems.

Though only a minority of site visitors may sign up for web-based alcohol programmes, nevertheless the numbers engaged can be very large, and the risk-reductions seem of the order typical in studies of brief advice to drinkers identified in health care settings. In these settings screening programmes typically identify people who are not actually seeking help for drinking problems – ‘pushing’ them towards intervention and change – while web sites ‘pull’ in people already curious or concerned about their drinking. As such these two gateways can play complementary roles in improving public health and offering change opportunities to people who would not present to alcohol treatment services. However, in Britain and elsewhere, both tactics reach only small fractions of the population who drinking excessively, leaving the bulk of the public health work to be done by interventions which drinkers generally cannot avoid and do not have seek out, such as price increases and availability restrictions.

With its combination of a randomised trial and a ‘real-world’ test, the featured research programme has gone further than any other in establishing the beneficial impacts of web-based alcohol interventions. However, largely because many site users do not complete research surveys, it remains impossible to be sure that the results seen in such studies will be replicated across the entire usership of the sites. Details below.

Strengths and limitations of the featured study
The featured study’s combination of a randomised trial with all its methodological safeguards, and a ‘real-world’ trial approximating normal conditions, affords what seems to be the best indication to date of the contribution web-based self-help interventions could make to reducing heavy drinking and associated health risks. However, its twin pillars are weakened by the fact that many people either did not join the studies or did not supply follow-up data; those who did may not have been typical of all the people who might access such sites.

In the randomised trial, 40% of the baseline sample did not complete the six-month follow-up survey, and in the featured study, nearly 60%. Though on the measures taken by the study the respondents generally seemed typical of the baseline sample, clearly something was sufficiently different to cause them to respond while the others did not. In both studies this problem was catered for by assuming that non-responders were also non-changers. Though this almost certainly underestimated the impact of the intervention, still in both there remained significant and worthwhile improvements.

What could not be catered for in either study was the degree to which people who join such studies differ from the much greater number who would use the web sites, but decline participation in research. This problem was especially apparent in the featured study, in which it seems that around 6% of site visitors signed up for the self-help programme. Of these, perhaps a third or slightly more of the people who signed up for the programme during the relevant period also agreed to participate in the research. In some important ways (including amount drunk and motivation to change) they seemed similar to the bulk of programme sign-ups, though the researchers suspect they were more likely to have engaged with the programme.

Opening more doors to change for more people
A review of computer-based alcohol services for the general public has rehearsed the advantages: immediate, convenient access for people (the majority in developed nations) connected to the internet; consequently able to capitalise on what may be fleeting resolve; anonymous services sidestep the embarrassment or stigma which might deter help-seeking; such services are available to people unwilling or less able to talk about their problems to a stranger; generally they are free and entail no travel costs or lost income due to time off work; very low operating cost per user if widely accessed; easily updated.

In consumption terms, the drinking problems of web site users are comparable to those of drinkers who seek treatment, yet few have received professional help, perhaps partly because their higher socioeconomic status and greater resources have enabled them to restrict the consequential damage. People who actually engage with web-based assessments of their drinking problems have more severe problems than those who just visit and leave. Including the randomised trial which paved the way for the featured study, the review found eight studies which evaluated the effectiveness of computer-based interventions for the general public.

In all but one the users significantly improved on at least one of the alcohol-related measures recorded by the studies.
A particular role for alcohol self-help sites may be to offer an easy, quick and accessible way to for drinkers to actualise their desire to tackle their problems, especially when that desire is allied with the resources to implement and sustain improvements without face-to-face or comprehensive assistance. After conducting the Project MATCH trial, some of the world’s leading alcohol treatment researchers argued that “access to treatment may be as important as the type of treatment available”. The implication is that in cultures which accept ‘treatment’ as a route to resolving unhealthy and/or undesirable drinking, having convincing-looking and accessible ‘treatment doors’ to go through may be more important than what lies behind those doors, as long as this fulfils the expectations of the client or patient. This is likely to be especially the case for people who retain a stake in conventional society in the form of marriages, jobs, families, and a reputation to lose. These populations – the kind the featured study suggests are attracted to self-help alcohol therapy web sites – have more of the ‘recovery capital’ resources needed to themselves do most of the work in curbing their drinking.

The British Down Your Drink site
The best known British alcohol self-help web site is the Down Your Drink site run by a team based at University College London, an initiative originally funded by the Alcohol Education and Research Council and now by the Medical Research Council’s National Prevention Research Initiative. In 2007 this was revised to offer set programmes from a one-hour brief intervention to several weeks, but also to generally give the user greater control over the use they made of the site. The approach remained based on principles and techniques derived from motivational interviewing and cognitive-behavioural therapies.

The previous version had been structured as six consecutive modules to be accessed weekly. An analysis of data provided by the first 10,000 people who registered at the site after piloting ended in September 2003 revealed that most were in their 30s and 40s, half were women, nearly two-thirds were married or living with a partner, just 4% were unemployed, and most reported occupations from higher socioeconomic strata.

As an earlier study commented, site users were predominantly middle class, middle aged, white and European. Six in 10 either did not start the programme, or completed just the first week. About 17% completed the six weeks. Of these, 57% returned an outcome questionnaire. Compared to their pre-programme status, on average they were now at substantially lower risk, and functioning better and living much improved lives.
The sample had been recruited over about 27 months, a registration rate of about 4500 a year. By way of comparison, in England during 2008/09, around 100,000 adults were treated for their alcohol problems at conventional services. User profile and site usage had been similar during the earlier pilot phase. Results from surveys sent to pilot programme completers indicated that three quarters had never previously sought help for their drinking.

Source: Published in Findings 19 May 2010 Alcoholism: Clinical and Experimental Research: 2009, 33(8), p. 1401–1408

Researchers at Uppsala University in Sweden studied the relationship between crime and steroid use in 1,440 Swedish residents tested for the drugs between 1995 and 2001 from clinics, including substance abuse facilities, as well as police and customs stations.

Of those involved in the study, 241 tested positive, with an average age of about 20.
The research team found those who tested positive for steroid use were roughly twice as likely to have been convicted of a weapons offense and one-and-a-half times as likely to have been convicted of fraud.

When the researchers excluded people from substance abuse facilities from their analysis the connection with armed crime remained, but the link between steroid use and fraud disappeared.
While steroids are linked with outbursts of uncontrolled violence known as “‘roid rage,” they did not appear to be connected with sexual offenses, violent crimes such as murder, assault and robbery, or crimes against property such as theft.

This investigation instead reveals that steroid use may be linked with premeditated crimes—those involving preparation and advance planning.
One explanation the researchers suggest for the findings is that criminals involved in serious crimes such as armed robbery or the collection of crime-related debts might benefit from the muscularity, heavy build and increase in aggression that comes with steroid use.

The scientists report their findings in the November issue of the Archives of General Psychiatry.

Source: Fox News Live Science Monday , November 06, 2006

More than 20 children and teenagers are being treated in hospital every day for alcohol-related illnesses, including mental disorders, poisoning and liver disease, according to newly released official data.

The figures, labelled “staggering” by one of Britain’s most senior doctors, show that in the year 2005-6, during which Labour introduced 24-hour drinking, the number of under-18s seeking treatment for alcohol-related health problems leapt by 13% to 8,894, an average of 24 a day.

The research, released in parliament by Caroline Flint, the health minister, shows that the number treated has gone up by 33% since Labour came to power in 1997.

Professor Ian Gilmore, president of the Royal College of Physicians, said: “This is a staggering rise and it is only the tip of the iceberg.
“Drinks sold by supermarkets and off-licences are cheaper than ever, and those shops have been at the front of the queue for 24-hour licences, so it has never been more available.

“The younger they drink, the more likely they are to have alcohol-related problems later in life. It is now commonplace to see men and women in their twenties with end-stage alcoholic liver damage.”
The disease figures released by Flint do not include those people treated for injuries sustained in incidents such as drunken fights or drink-driving.

Separately, the government has released figures for patients treated for alcohol-related conditions in accident and emergency wards, showing that alcohol-related medical emergencies and hospital treatments have doubled since 1997.

In some parts of the country the rise is even steeper. The worst areas include the region formerly covered by Cheshire and Merseyside Strategic Health Authority, where 742 young people were treated last year, a rise of more than 25% in just a year. In Northumberland, Tyne and Wear, the number went up by a quarter.
By contrast, some southern health authorities experienced an improvement. In Bedfordshire and Hertfordshire, for example, there were only 119 cases, a fall of 30%.

In addition to the figures for children and teenagers, the Department of Health data also show that the number of people aged 18 and over treated for alcohol-related illness has gone up from 124,925 to 253,603 since 1997, a rise of more than 100%.
The data, released in a written answer, appear to contradict the government’s claims that the liberalisation of pub opening and supermarket off-sales time would lead to more responsible drinking.

They bear out research published earlier this year by the British Association for Emergency Medicine, which found an increase in alcohol-related injuries treated in hospital among all age groups since the change to the drinking laws.

Ahead of its launch of 24-hour opening in November 2005, the government assured voters that there would be tougher controls on underage drinking.
It announced on-the-spot fines for children buying alcohol and tougher penalties for staff serving them.
Tessa Jowell, the culture secretary, said at the time: “The result will be more freedom for responsible adults and tougher treatment for the yobbish minority.”

Labour’s approach to teenage drinking has not always lived up to the responsible image that it likes to project.
In the run-up to the 2001 general election, the party sent text messages to first-time voters telling them, “Don’t give a XXXX for last orders? Vote Labour”. This was an allusion to advertisements for Castlemaine XXXX, the Australian beer.

Dr Gray Smith-Laing, a consultant at the Medway Maritime hospital in Gillingham, Kent, who treats patients with liver disease, said last week: “What we’re seeing is the numbers going up, the age coming down.

“The idea that (24-hour opening) just smooths out the drinking and people drink the same amount over a longer period of time is complete rubbish.”
The Department of Health says that levels of binge drinking have peaked and new facilities such as walk-in centres could explain the growth in treatment for drink-related injuries.

The department said yesterday: “The increased attendances at A&E departments, as seen in recently published figures, began some years ago. Evidence suggests that increased rate of growth of attendances predates the change in licensing laws by several years. In fact, this year growth has actually slowed.”

SOURCE: POSTED BY ALCOHOLICS ANONYMOUS UK AT 7:50 AM MON 25.12.06

Results will be published in the July 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“In spite of their differences in pharmacology, alcohol and tobacco consumption are often intimately linked,” said Traute Flatscher-Bader, a postdoctoral research fellow at The University of Queensland and corresponding author for the study. “Nonetheless, the molecular mechanisms that underlie alcohol and nicotine abuse, and particularly their co-abuse, are still incompletely understood.”

“One thing that researchers have encountered is that it is often difficult to find ‘pure’ alcoholics, that is, alcoholics that only abuse alcohol and nothing else,” agreed Simon Worrall, director of postgraduate coursework programs in molecular biology at The University of Queensland. “Many alcoholics are poly-drug abusers, with the most common other drug being nicotine. Thus, many studies which have studied the effects of alcohol on the brain and other organs have been compromised because they have not taken account of the effects of nicotine addiction which is often superimposed on the effects of alcohol addiction.”

In the first part of the current study, Flatscher-Bader and her colleagues used DNA microarray technique to study the expression of many thousands of genes in the brains of non-smoking and smoking alcoholics and non-drinking smokers.

“We examined the impact of alcoholism and smoking on gene expression in the NAC in 20 chronic alcohol abusers and controls with and without recent smoking history,” said Flatscher-Bader. “The results revealed that in this brain region, the abuse of alcohol and nicotine had distinct effects on the expression of genes. In addition, altered expression of a number of genes was associated with both alcohol and nicotine abuse. Within the latter group was a set of genes which play a crucial role in a molecular pathway regulating cell structure.”

The researchers then went on to investigate in more detail the altered expression of six selected genes within the pathway regulating cell structure in two brain regions, using 30 cases comprised again of smoking and non-smoking controls and alcohol abusers. For this part of the study they used the method called “real time polymerase chain reaction.”

“This expanded investigation revealed that one of the genes, called RHOA, was elevated by alcohol abuse and its highest expression was evident in the smoking alcoholics in both brain regions,” said Flatscher-Bader. “The RHOA gene had previously been implicated in the initiation of tobacco smoking. In the NAC, the expression of a further four of the six selected genes was increased by alcohol abuse. Interestingly, the highest expression for each of the genes in the NAC was in the smoking alcoholics. In the other brain region called the VTA, alcohol abuse had a similar effect and elevated the expression of all six selected genes. In contrast to the NAC, however, concurrent smoking dampened the induction of five of these alcohol-sensitive genes in the VTA.”

“Many studies have analyzed the changes in gene expression in this brain system to try to untangle the molecular pathology of alcohol addiction,” said Worrall, “but this is amongst the first to take into account the effect of co-administration of nicotine with alcohol.

Flatscher-Bader stressed that there are several cell types in the brain and there are several steps between gene expression and impact on cell structure and function. “It has to be emphasized that our study is important as a first step in identifying molecular pathways underlying the effects of alcohol abuse and smoking and their co-joint abuse on the human NAC and VTA, “she said. “It now needs to be tested if our findings are, indeed, associated with changes to neuronal structure and function.”

“A better understanding of the molecular basis of withdrawal may help in the development of new treatments to ameliorate the symptoms,” added Dr Worrall. “Not many previous studies took into account the potential effects of nicotine addiction that may be superimposed on top of those from alcohol, so these results may help clinicians better use present therapy/drugs to treat patients abusing both alcohol and/or nicotine and may also lead to the development of new drugs.”

Source: www.medicalnewstoday.com 5.5.2010

]]> http://drugprevent.org.uk/ppp/2010/08/separate-and-joint-effects-of-alcohol-and-tobacco-on-the-nucleus-accumbens/feed/ 0 http://drugprevent.org.uk/ppp/2010/07/parents-know-warning-signs-of-drug-abuse/ http://drugprevent.org.uk/ppp/2010/07/parents-know-warning-signs-of-drug-abuse/#comments Tue, 27 Jul 2010 15:18:36 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6937 Q: How can I tell if my child has been using marijuana?
A: There are some signs you might be able to see. If someone is high on marijuana, he or she might:

• Seem dizzy and have trouble walking;
• Seem silly and giggly for no reason;
• Save very red, bloodshot eyes; and
• Have a hard time remembering things that just happened.

When the early effects fade, the user can become very sleepy.

Parents should be aware of changes in their child’s behavior, although this may be difficult with teens. Parents should look for withdrawal, depression, fatigue, carelessness with grooming, hostility and deteriorating relationships with family members and friends.

In addition, changes in academic performance, increased absenteeism or truancy, lost interest in sports or other favorite activities, and changes in eating or sleeping habits could be related to drug use. However, these signs may also indicate problems other than using drugs.

In addition, parents should be aware of:

• Signs of drugs and drug paraphernalia, including pipes and rolling papers;
• Odor on clothes and in the bedroom;
• Use of incense and other deodorizers;
• Use of eye drops; and
• Clothing, posters, jewelry, etc., promoting drug use.

Source: The National Institute on Drug Abuse 2010

]]> http://drugprevent.org.uk/ppp/2010/07/parents-know-warning-signs-of-drug-abuse/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/alcohol-binge-drinking-linked-to-increased-hypomania-risk/ http://drugprevent.org.uk/ppp/2010/05/alcohol-binge-drinking-linked-to-increased-hypomania-risk/#comments Fri, 07 May 2010 12:55:31 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6685 Young men who report an unstable pattern of alcohol consumption including binge drinking have an elevated risk for experiencing hypomania, study results show. Notably, the effect was independent of total alcohol consumption and the presence of clinical alcohol use disorders.
“This fits with the idea that instability in different biological and behavioral systems is a core feature of risk for hypomania and finally risk for bipolar disorders,” say study authors Thomas Meyer (Newcastle University, UK) and Larissa Wolkenstein (University of Tübingen, Germany) in the journal Comprehensive Psychiatry.
Recent studies have suggested that vulnerability to hypomania is related to instability in certain psychologic processes. For example, individuals at risk for hypomania do not generally sleep less than others, but report a much more unstable sleeping pattern. Similarly fluctuations in self-esteem are much more characteristic of vulnerability to hypomania than are consistently low or high levels of self-esteem.
In the current study, the researchers assessed whether alcohol use might show a similar relationship to hypomania. They recruited 120 male students who completed the Hypomanic Personality Scale and were independently interviewed with the FORM 90 to assess alcohol consumption. The latter comprised an interview about a typical weekly drinking pattern and a calendar to assess drinking behavior over the last 90 days, noting special days with unusual drinking behavior.
The researchers found that intra-individual fluctuations in alcohol consumption predicted hypomania after accounting for clinical diagnoses of abuse or dependency. In addition, vulnerability for hypomania was significantly associated with mean standard ethanol content per drinking day.
Discussing their findings, the researchers note a recent theory that bipolar disorder is related to a hypersensitivity to reward-related cues, which is due to a dysregulation of the behavioral activation system.
“To extend this work further, it would be reasonable to look more closely at the motivational and affective processes associated with drinking alcohol and bipolar disorder and how mood and drinking are related,” Meyer and Wolkenstein comment.
Source: MedWire (www.medwire-news.md) 19 March 2010
]]> http://drugprevent.org.uk/ppp/2010/05/alcohol-binge-drinking-linked-to-increased-hypomania-risk/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/brain-damage-kills-craving-for-nicotine/ http://drugprevent.org.uk/ppp/2010/05/brain-damage-kills-craving-for-nicotine/#comments Sat, 01 May 2010 11:51:49 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6588 SMOKERS who suffer damage to a particular part of their brains appear to be able to quit their nicotine habit easily – a discovery that might open new avenues of addiction research.
A study of smokers who had suffered brain damage of various kinds after a stroke showed that those with injuries to a part of the brain called the insula were in many cases able to quit smoking quickly and easily – saying they had lost the urge to smoke altogether.
The insula receives information from the body and translates it into subjective feelings such as hunger, pain and craving, including craving for drugs.
However, the insula has not attracted much attention in studies on drug addiction, according to the research in the latest edition of the journal Science.
Deliberately damaging people’s insulas is not considered a realistic treatment option, because the risks are too great and the insula also has a role in many essential functions, such as the desire to eat.
But in the long term, the authors said, drugs might be developed to target the insula.
Other techniques for affecting the insula might in future also include electrical stimulation, already used in patients with depression. However, current techniques cannot penetrate the brain deeply enough to reach the insula.
The study was inspired by the experience of a man who had smoked 40 cigarettes a day before his insula was damaged in a stroke. He quit smoking immediately after, telling researchers his body “forgot the urge to smoke”.
Additional reporting: The Times

Source: news.com.au January 27th 2007


]]> http://drugprevent.org.uk/ppp/2010/05/brain-damage-kills-craving-for-nicotine/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/anterior-cingulate-grey-matter-deficits-and-cannabis-use-in-first-episode-schizophrenia/ http://drugprevent.org.uk/ppp/2010/05/anterior-cingulate-grey-matter-deficits-and-cannabis-use-in-first-episode-schizophrenia/#comments Sat, 01 May 2010 11:47:07 +0000 ndpa http://drugprevent.org.uk/ppp/2010/05/anterior-cingulate-grey-matter-deficits-and-cannabis-use-in-first-episode-schizophrenia/ Research Summary

Background

Despite the high prevalence of cannabis use in schizophrenia, few studies have examined the potential relationship between cannabis exposure and brain structural abnormalities in schizophrenia.
Aims To investigate prefrontal grey and white matter regions in patients experiencing a first episode of schizophrenia with an additional diagnosis of cannabis use or dependence (n=20) compared with similar patients with no cannabis use (n=31) and healthy volunteers (n=56).
Method Volumes of the superior frontal gyrus, anterior cingulate gyrus and orbital frontal lobe were outlined manually from contiguous magnetic resonance images and automatically segmented into grey and white matter.
Results Patients who used cannabis had less anterior cingulate grey matter compared with both patients who did not use cannabis and healthy volunteers.
Conclusions A defect in the anterior cingulate is associated with a history of cannabis use among patients experiencing a first episode of schizophrenia and could have a role in poor decision-making and in choosing more risky outcomes.
Philip R. Szeszko, PhD, Delbert G. Robinson, MD and Serge Sevy, MD et al
Correspondence: Dr Philip R. Szeszko, Zucker Hillside Hospital, Psychiatry Research, 75–59 263rd Street, Glen Oaks, NY11004, USA. Tel: +1 718 470 8489; fax: +1 718 343 1659; email: szeszko@lij.edu

Source: The British Journal of Psychiatry (2007) 190: 230-236. doi: 10.1192/bjp.bp.106.024521
© 2007 The Royal College of Psychiatrists

James M. Howard,
Independent Biologist

It is my hypothesis that schizophrenia results from reduced fetal brain growth and development due to low maternal DHEA. This is exposed later in life by hormones that interfere with DHEA availability, that is, cortisol and testosterone, along with the natural decline of DHEA that begins around age twenty. Therefore, schizophrenia often occurs following a stressful event (cortisol) in the late teens or early twenties (testosterone and loss of DHEA) or later in life as DHEA reaches very low levels. Schizophrenia is characterized by low DHEA. Individuals with normal DHEA along with reduced fetal DHEA may not develop schizophrenia.
I suggest that the psychoactive chemicals of cannabis exert their effects by binding to androgen receptors. It has been found that THC and CBN inhibit binding of dihydrotestosterone to the androgen receptor (Endocrinology 1980; 107: 848-50). This binding to receptors in the advanced forebrain would reduce executive function and increase lower brain function by redistributing DHEA. That is, blocking access to upper brain receptors would increase lower brain function and increase lower brain functions such as appetite, etc.
DHEA binds to the androgen receptor. Cannabis use would reduce DHEA binding to the androgen receptor. It is this blocking of DHEA at its upper level receptors and subsequent redistribution of availability for lower brain activity that I think produces the effects of cannabis.
It is known that DHEA directly affects the anterior cingulate cortex (Psychopharmacology (Berl) 2006; 188: 541-51). Interference of DHEA binding in the anterior cingulate cortex of individuals with reduced growth and development in this area may reduce both function and maintenance of this area with the result being the symptoms of schizophrenia.

]]> http://drugprevent.org.uk/ppp/2010/05/anterior-cingulate-grey-matter-deficits-and-cannabis-use-in-first-episode-schizophrenia/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/behavioral-response-to-novelty-foreshadows-neurological-response-to-cocaine/ http://drugprevent.org.uk/ppp/2010/05/behavioral-response-to-novelty-foreshadows-neurological-response-to-cocaine/#comments Sat, 01 May 2010 11:46:06 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6576 BY LORI WHITTEN, NIDA Notes Staff Writer

NIDA-supported researchers Dr. Cheryl Kirstein and Ms. Kirstie Stansfield at the University of South Florida have found that higher scores on tests of impulsivity and some behavioral responses to novelty correlate with a heightened biological response to cocaine in adolescent, but not adult, rats. The findings accord well with scientists’ widely shared view that developmental differences in brain systems that use the neurotransmitter dopamine underlie age differences in susceptibility to drug abuse.
Dr. Kirstein and Ms. Stansfield conducted a series of behavioral assays to rate rats’ relative responsiveness to novelty, then compared these results with measures of dopamine release in the reward pathway after an injection of cocaine. First, they put adolescent rats (34 days old, which is roughly equivalent to adolescence in people) and fully mature rats (59 days old, equivalent to human young adulthood) through four behavioral protocols. The tests measured activity in a new environment (how much the rat moved around when put into a new cage); impulsivity (how quickly it approached a new object placed into its cage); exploratory drive in response to a new object (how many times it approached the object in a given period of time); and attraction to new objects (what percentage of a given time interval was spent close to the object).
The researchers then injected the animals with saline and then, 2 hours later, with cocaine 20 mg/kg. Every 10 minutes, starting immediately after the saline injection and continuing until 2 hours after administering the cocaine, they measured the concentrations of the neurotransmitter dopamine and its major metabolite in the rats’ nucleus accumbens (NAc). The measurements were made using the technique of in vivo microdialysis. By the time of the last measurement, the drug had cleared the animal’s system.
ON MOST TESTS, AGE MATTERS
In their analysis, the researchers compared cocaine-induced dopamine release in animals that had responded above the mean level on each test (high responders, HR) to those who had scored below the mean (low responders, LR). The results revealed that among both the adult and adolescent rats, those that exhibited greater activity in a new environment also demonstrated enhanced dopamine release following a cocaine injection. This was the only test, however, in which age did not influence cocaine-induced dopamine release. The other behavioral assays revealed interactions between age and the response to novelty on cocaine-induced dopamine release in the NAc:
• Impulsivity—Adolescent rats with above-the-mean impulsivity scores released more dopamine in response to cocaine than their age mates who were LR. Mature rats exhibited no clear relationship between impulsivity and cocaine-induced dopamine response.
• Exploration of a new object—Adolescent rats with above-the-mean scores on this measure released more dopamine in response to cocaine than their age mates who were LR. Adult rats showed the opposite pattern: Animals with above-the-mean scores showed attenuated cocaine-induced dopamine release compared with age mates who were LR.
• Attraction to a new object—Adolescent rats exhibited no clear relationship between reactivity on this assay and cocaine-induced dopamine release. Mature rats with above-the-mean scores released less dopamine in response to cocaine compared with their age mates who were LR.
Dr. Kirstein’s finding that for all the animals, greater activity in a new environment corresponded with increased sensitivity to stimulants is consistent with earlier research. Her team’s mixed findings on the impulsivity and other novelty response tests indicates, she says, that those behaviors arise from different physiological mechanisms than does locomotor activity. “My colleagues and I think locomotor activity may reflect primarily dopamine activity in a brain circuit involved with generating and controlling movement. Novelty may instead differentially stimulate mesolimbic dopamine—a pathway implicated in attention as well as reward and motivation,” says Dr. Kirstein.
In Vivo Microdialysis
The investigators used In Vivo microdialysis to measure dopamine each animal released from its nucleus accumbens (NAc) in response to cocaine. They implanted a probe into the shell area of the NAc. The probe is a fine tube, about the size of a sewing needle, connected to a mini-pump that continuously perfuses it with artificial cerebrospinal fluid. The membrane tip of the probe captures dopamine and its metabolites. The samples collected by the needle are then analyzed using techniques, such as chromatography, that are able to isolate dopamine and its metabolites from other molecules.
INHIBITION DEVELOPS LATER
The findings on the three tests where age affected the relationship between behavior and cocaine-induced dopamine release may reflect maturation of the brain’s reward circuit. When rats are adolescents, dopamine-producing and releasing cells in this circuit may be particularly sensitive both to novelty and to pharmacological stimulation. As part of normal neurological development, areas of the brain that dampen the activity of this circuit come “online” later, explaining the age-related differences observed in Dr. Kirstein’s study. “The mesolimbic pathway and the cortical areas that inhibit it to regulate dopamine release are not yet fully matured in the adolescent, and this may explain why the adolescent brain responds to drugs differently than the adult brain,” says Dr. Kirstein.
“The results of Dr. Kirstein’s study, along with other animal research on the interaction of drugs and developmental stage, indicate that the adolescent brain is more responsive to drugs than the adult brain—both neurochemically and behaviorally,” says Dr. Nancy Pilotte of NIDA’s Division of Basic Neuroscience and Behavioral Research. Studies that identify the physiological and behavioral processes underlying age-related susceptibility to addiction complement epidemiological work on the individual and social factors contributing to adolescent vulnerability to substance abuse.

SOURCE NIDA Notes Vol. 21, No. 2 (February 2007)
Stansfield, K.H., and Kirstein, C.L. Neurochemical effects of cocaine in adolescence compared to adulthood. Developmental Brain Research 159(2):119-125, 2005.



]]> http://drugprevent.org.uk/ppp/2010/05/behavioral-response-to-novelty-foreshadows-neurological-response-to-cocaine/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/neurobiological-effects-of-early-life-cannabis-exposure-in-relation-to-the-gateway-hypothesis-2/ http://drugprevent.org.uk/ppp/2010/05/neurobiological-effects-of-early-life-cannabis-exposure-in-relation-to-the-gateway-hypothesis-2/#comments Sat, 01 May 2010 11:44:51 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6574 <span style=”font-size: 10pt; font-family: Verdana;”> Abstract: The use of Cannabis sativa preparations, such as hashish and marijuana, is wide-spread among young people, including pregnant women. Despite this concern, the consequences of cannabis exposure on the brain during periods of active brain development, such as the prenatal phase and adolescence, is not well known. Several epidemiological studies support the cannabis gateway hypothesis, where early cannabis use is suggested to increase the risk of initiating use of other illicit drugs, e.g., amphetamine or heroin. However, the nature of such direct links are unclear. Therefore, the aim of this thesis was to test experimentally the cannabis gateway hypothesis, i.e., to determine whether cannabis exposure during periods of active brain development alters reward-related behavior and neurobiology for psychostimulant and opioid drugs by the use of animal models.
In the first study, we examined the effects of early adolescent exposure (postnatal day; PND; 28-32, one injection per day) with the synthetic cannabinoid CB1 receptor agonist WIN55,212-2 and the main psychoactive substance in C. sativa, Δ9-tetrahydrocannabinol (THC) on amphetamine-induced motor behavior and dopamine release in the nucleus accumbens during adolescence. No alterations were evident in the cannabinoid exposed rats, results which did not support the cannabis gateway hypothesis in relation to subsequent psychostimulant abuse.
Next, we investigated the effects of adolescent exposure on subsequent opioid reward-related behavior and the neurobiology of opioid and cannabinoid systems during adulthood. We studied THC exposure across the full adolescent period (PND 28-49), and administered the drug once every third day in order to better mimic the pattern of intermittent use seen in teenagers. The results revealed discrete opioid-related alterations within brain regions highly implicated in reward and hedonic processing (e.g., increased proenkephalin gene expression in the nucleus accumbens and increased mu opioid receptors in the ventral tegmental area). This was coupled to increased heroin intake in a self-administration paradigm and increased morphine conditioned place preference, indicating altered sensitivity to the reinforcing properties of opioids.
Furthermore, in evaluating the adolescent ontogeny of the opioid and cannabinoid systems within limbic-related brain areas, we found that active endocannabinoid- and opioid- related neurodevelopment takes place to a very high extent during this period. Most pronounced were the alterations in endocannabinoid levels in cognitive brain areas, even though alterations were also apparent in reward-related regions.
Finally, we investigated the effects of prenatal cannabis exposure (gestational day 5- PND 2) on subsequent opioid reward-related behavior and neurobiology of the opioid and cannabinoid systems in adulthood. Similar to adolescent cannabis exposure, prenatal exposure induced discrete opioid-related alterations within brain regions highly implicated in reward and hedonic processing. Moreover, elevated heroin-seeking observed during extinction and after food deprivation was evident in the THC exposed rats, suggesting an increased motivation for drug use under conditions of stress.
Taken together, this thesis presents neurobiological support for the cannabis gateway hypothesis in terms of adult opiate, but not amphetamine, abuse, with underlying long-term disturbances of discrete opioid-related systems within limbic brain regions.

<em>Source: Ellgren, Maria Karolinksa Institute Sweden ISBN: 978-91-7357-064-0  Feb.2007
</em>
<span style=”font-size: 10pt; font-family: Verdana;”>

]]> http://drugprevent.org.uk/ppp/2010/05/neurobiological-effects-of-early-life-cannabis-exposure-in-relation-to-the-gateway-hypothesis-2/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/new-study-confirms-dopamine-depletion/ http://drugprevent.org.uk/ppp/2010/05/new-study-confirms-dopamine-depletion/#comments Sat, 01 May 2010 11:40:20 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6564 A researcher at the University of Buffalo’s Research Institute on Addictions (RIA) has found a change in the brain that occurs after drug use and that may contribute to drug addiction.
The finding, reported in the January issue of Biological Psychiatry, demonstrates that repeated exposure to different types of drugs of abuse, such as cocaine, nicotine, amphetamine and alcohol, lead to a persistent or long-term reduction in the electrical activity of dopamine neurons in the brain.
Dopamine neurons are the origin of the reward pathway responsible for the “feel good” experience that is such a strong component of drug use and abuse.
“A persistent reduction in dopamine neuron electrical activity after repeated exposure to different types of drugs appears to be the result of excessive excitation of dopamine neurons,” according to Roh-Yu Shen (photo), a neuroscientist and the lead investigator on the study. “This represents a new and potentially critical neural mechanism for addiction and provides a working model that suggests how the reward pathway function is altered and how these changes can be responsible for triggering intense craving and compulsive drug-seeking.”

Source. January 2007 issue of Biological Psychiatry



]]> http://drugprevent.org.uk/ppp/2010/05/new-study-confirms-dopamine-depletion/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/abstinence-regenerates-alcoholic-brain/ http://drugprevent.org.uk/ppp/2010/05/abstinence-regenerates-alcoholic-brain/#comments Sat, 01 May 2010 11:38:44 +0000 ndpa http://drugprevent.org.uk/ppp/2010/05/abstinence-regenerates-alcoholic-brain/ The brains of alcoholics can show measurable improvement in volume, chemical activity, and functionality after as little as seven weeks of abstinence, a new study published in the journal Brain today reveals.

Researchers from Germany, the UK, Switzerland and Italy collaborated on a study of ten men and five women alcoholics who had achieved an average of 38 days abstinence at the time of the study. Alcoholics who used psychoactive medications or who smoked more than 10 cigarettes a day after they stopped drinking were excluded from the data. Researchers used functional magnetic resonance imaging (fMRI) and proton MR spectroscopy, laboratory tests for levels of brain chemicals that measure nerve integrity and repair, and performance tests for attention and concentration.

Brain volume increased an average of two percent, researchers found, and there were major increases in the substances that measured nerve health and regrowth. There were also improvements in performance. However, in one subject, who had the longest history of alcoholism in the study (more than 25 years), the evidence of brain recovery was not visible within the relatively short time span of the study.

The leader of the research, Dr Andreas Bartsch from the University of Wuerzburg, Germany, said:
“The core message from this study is that, for alcoholics, abstinence pays off and enables the brain to regain some substance and to perform better. However, our research also provides evidence that the longer you drink excessively, the more you risk losing this capacity for regeneration. Therefore, alcoholics must not put off the time when they decide to seek help and stop drinking; the sooner they do it, the better.”

Source. Journal ‘Brain’ SUNDAY, DECEMBER 17, 2006



]]> http://drugprevent.org.uk/ppp/2010/05/abstinence-regenerates-alcoholic-brain/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/brain-scans-reveal-cause-of-smokers-cravings/ http://drugprevent.org.uk/ppp/2010/05/brain-scans-reveal-cause-of-smokers-cravings/#comments Sat, 01 May 2010 11:37:05 +0000 ndpa http://drugprevent.org.uk/ppp/2010/05/brain-scans-reveal-cause-of-smokers-cravings/ Summary

DURHAM, N.C. — Within the mind of every smoker trying to quit rages a battle between the higher-order functions of the brain wanting to break the habit and the lower-order functions screaming for another cigarette, say researchers at Duke University Medical Center. More often than not, that cigarette gets lit.
Brain scans of smokers studied by the researchers revealed three specific regions deep within the brain that appear to control dependence on nicotine and craving for cigarettes. These regions play important roles in some of the key motivations for smoking: to calm down when stressed, to achieve pleasure and to help concentration.
“If you can’t calm down, can’t derive pleasure and can’t control yourself or concentrate, then it will be extremely difficult for you to break the habit,” said lead study investigator Jed E. Rose, Ph.D., director of the Duke Center for Nicotine and Smoking Cessation Research. “These brain regions may explain why most people try to quit several times before they are successful.”
Understanding how the brain responds to cigarette cravings can help doctors change nicotine cessation treatments to address all three of these components of withdrawal, Rose said. Drugs or therapies that target these regions may help smokers stave off the cravings that often spoil their attempts to quit.
The team’s findings are now online in the journal Neuropsychopharmacology. The research was funded by Phillip Morris USA.
Approximately one in five Americans smokes. Even though 70 percent of smokers report that they would like to quit, only 5 percent do so successfully.
In this study, the researchers manipulated the levels of nicotine dependence and cigarette craving among 15 smokers and then scanned their brains using positron emission tomography, or PET scans, to see which areas of the brain were most active.
Three specific regions of the brain demonstrated changes in activity when the smokers craved cigarettes versus when they did not.
One region that lights up, called the thalamus, is considered to be the key relay point for sensory information flowing into the brain. Some of the symptoms of withdrawal among people trying to quit stem from the inability to focus thoughts and the feeling of being overwhelmed, and could thus be explained by changes in this region, according to the researchers. The researchers found that changes in this region were most dramatic among those who said they smoked to calm down when under stress.
Another region that lights up is a part of the pleasure system of the brain. Changes in this region, called the striatum, were most notable in people who smoked to satisfy craving and for pleasurable relaxation, the researchers said.
A third region that lights up, called the anterior cingulate cortex, is vital to cognitive functions such as conflict, self regulation, decision making and emotion. People whose brain scans showed the most differences in this region also reported that they smoked to manage their weight.
“This knowledge gives us new clues about brain mechanisms underlying addiction to cigarettes and could allow us design better methods to help smokers quit,” Rose said.
Rose and his colleagues are now planning to perform brain scans on smokers undergoing nicotine replacement therapy, such as the nicotine patch, to determine how these treatments affect the same regions of the brain.
Other researchers participating in the study were Frederique M. Behm, Alfred N. Salley, James E. Bates, R. Edward Coleman, Thomas C. Hawk and Timothy G. Turkington.

Source: www.dukemednews March 2007


]]> http://drugprevent.org.uk/ppp/2010/05/brain-scans-reveal-cause-of-smokers-cravings/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/prospective-memory-loss-linked-to-teenage-alcohol-abuse/ http://drugprevent.org.uk/ppp/2010/05/prospective-memory-loss-linked-to-teenage-alcohol-abuse/#comments Sat, 01 May 2010 11:32:00 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6549 Summary

Heavy drinking and smoking as teenagers may damage the ability to remember future tasks, according to new research.
The findings are drawn from two studies exploring teenagers’ capacity for prospective memory – the ability to remember something you had intended to do in the future, such as returning a phone call or paying a bill on time.
In one study, 108 students aged 16 to 19 years old were asked to report the number of times that prospective memory had failed them recently. Teenagers who were “excessive” alcohol users were significantly less likely to remember future tasks, the researchers found.
A second study found that teenage smokers reported more memory lapses in general than non-smokers, and also reported fewer items in a prospective memory test.
The findings are being presented today at the British Psychology Society’s annual conference at the University of York.
The society said that although evidence exists suggesting alcohol abuse has a detrimental effect on memory for past events, little was known before now about its impact on prospective memory.
Thomas Heffernan of the University of Northumbria, who led the research, said: “The teenage years are important for structural and functional development of the brain.
“If our findings are confirmed, they suggest that heavy drinking and smoking in the teenage years may impede this important development. This may lead to greater problems with memory later in life.”

Source:Thursday March 22, 2007 SocietyGuardian.co.uk



]]> http://drugprevent.org.uk/ppp/2010/05/prospective-memory-loss-linked-to-teenage-alcohol-abuse/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/researchers-say-smokers-cost-employers-in-missed-work-days-poor-performance/ http://drugprevent.org.uk/ppp/2010/05/researchers-say-smokers-cost-employers-in-missed-work-days-poor-performance/#comments Sat, 01 May 2010 11:29:47 +0000 ndpa http://drugprevent.org.uk/ppp/2010/05/researchers-say-smokers-cost-employers-in-missed-work-days-poor-performance/ Research Summary
A pair of new studies find that smokers take many more sick days annually than nonsmokers and perform worse when they are on the job, Bloomberg News reported March 29.
A Swedish study by Petter Lundborg and colleagues from Free University of Amsterdam found that smokers took an average of 34 sick days per year, compared to 20 per year for people who never smoked and 25 per year among former smokers.
Sweden has one of the highest rates of sickness absence in the industrialized world; in the U.S., the average worker takes off nine days annually for illness. “The results suggest that policies that reduce and/or prevent smoking may also reduce the number of days of sick leave,” wrote Lundborg.
In a study of women in the U.S. Navy, San Diego State University researcher Terry Conway and colleagues found that smokers were more likely to be discharged for medical reasons, bad behavior, misconduct, drug misuse and personality disorders. Smokers also were more apt to resign from the Navy before serving their full terms, and were paid less.
However, noted Conway, “Cigarette smoking might simply be a marker for other underlying factors such as nonconformity and high risk-taking, that contribute to poorer performance.”
The research was published in the journal Tobacco Control.

Source: Bloomberg News March 29 2007


]]> http://drugprevent.org.uk/ppp/2010/05/researchers-say-smokers-cost-employers-in-missed-work-days-poor-performance/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/cannabis-disrupts-brain-centre/ http://drugprevent.org.uk/ppp/2010/05/cannabis-disrupts-brain-centre/#comments Sat, 01 May 2010 11:20:19 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6529
Scientists have shown how cannabis may trigger psychotic illnesses such as schizophrenia.
A King’s College London team gave healthy volunteers the active ingredient tetrahydrocannabinol (THC).
They then recorded reduced activity in an area of the brain which keeps inappropriate thoughts at bay. THC levels are thought to have doubled in street cannabis in recent years – at the expense of other ingredients which may have a beneficial effect.

A separate study has shown that one of these ingredients – cannabidiol (CBD) – has the potential to dampen down psychotic symptoms, and could form the basis of new treatments. The research will be discussed at a conference on the impact of cannabis use to be held at the Institute of Psychiatry at King’s College this week.
Dependency
Although figures are not kept, it is estimated that as many as 500,000 people in the UK may be dependent on cannabis. Increasing numbers of people are seeking help for cannabis problems at specialist clinics. In 2005, only heroin users accounted for a greater proportion of patients. Experts are concerned that street cannabis is becoming increasingly potent. It is thought that average THC content has risen from 6% to 12% in recent years.
The Institute of Psychiatry study gave THC, CBD or placebo capsules to adult male volunteers who had not abused cannabis. They then carried out brain scans, and a battery of tests, and found that those who took THC showed reduced activity in an area of the brain called the inferior frontal cortex, which keeps inappropriate thoughts and behaviour, such as swearing and paranoia in check.
The effects were short-lived, but some people appeared more vulnerable than others.
In a second study, a team from Yale University administered THC intravenously. Even at relatively low doses, they found 50% of healthy volunteers began to show symptoms of psychosis. Volunteers who already had a history of psychotic symptoms appeared to be particularly vulnerable.
Side effects
A third study, by the University of Cologne, compared the effect of CBD and a commonly used anti-psychotic medicine, Amisulpride, on 42 patients with a history of schizophrenia.
After four weeks both groups showed a reduction in psychotic symptoms, but the CBD group were less prone to side effects, such as muscle stiffness and weight gain.

The researchers warned that THC and CBD compete with each other biochemically, so a rise in THC levels would blunt any positive impact of CBD. Professor Robin Murray, a consultant psychiatrist at the Institute of Psychiatry, said the research provided the strongest evidence that cannabis had a significant impact on the brain.
He said proving a long-term effect was extremely difficult, as it was not ethical or feasible to stimulate long-term psychosis in volunteers.
However, he said: “If something has an active effect in inducing the symptoms of psychosis after one dose, then it would not be at all surprising if repeated use induced the chronic condition.”
Professor Murray also warned that the high potency cannabis now widely available was likely to pose a much bigger risk to health than the significantly weaker formulations of previous years. “It is similar to comparing the effect of drinking a glass of wine at the weekend with drinking a bottle of vodka every day.”
Marjorie Wallace, of the mental health charity Sane, called the research a “significant contribution” to the understanding of the dangers of cannabis.
“Sane has been saying for years that there is a link between psychosis and the drug, particularly in its more potent forms.
“We strongly urge the government to heed the growing evidence and take urgent action to warn young people that some of them are risking lifelong mental illness – that they are playing Russian roulette with their minds.”

Source: BBC NEWS: 2007/04/30



]]> http://drugprevent.org.uk/ppp/2010/05/cannabis-disrupts-brain-centre/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/subtypes-of-alcoholism-discovered/ http://drugprevent.org.uk/ppp/2010/05/subtypes-of-alcoholism-discovered/#comments Sat, 01 May 2010 11:10:51 +0000 ndpa http://drugprevent.org.uk/ppp/2010/05/subtypes-of-alcoholism-discovered/
Analysis of a national sample of individuals with alcohol dependence (alcoholism) revealed five distinct subtypes of the disease. This finding should help dispel the myth that alcoholism is easily categorized and that an individual can be classified as a ‘typical alcoholic’.
Scientists at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health (NIH) report their finding in the journal Drug and Alcohol Dependence.
“Our findings should help dispel the popular notion of the ‘typical alcoholic,’” notes first author Howard B. Moss, M.D., NIAAA Associate Director for Clinical and Translational Research.
“We find that young adults comprise the largest group of alcoholics in this country, and nearly 20 percent of alcoholics are highly functional and well-educated with good incomes.
“More than half of the alcoholics in the United States have no multigenerational family history of the disease, suggesting that their form of alcoholism was unlikely to have genetic causes.”
“Clinicians have long recognized diverse manifestations of alcoholism,” adds NIAAA Director Ting-Kai Li, M.D, “and researchers have tried to understand why some alcoholics improve with specific medications and psychotherapies while others do not. The classification system described in this study will have broad application in both clinical and research settings.”
Previous efforts to identify alcoholism subtypes focused primarily on individuals who were hospitalized or otherwise receiving treatment for their alcoholism.
However, recent reports from NIAAA’s National Epidemiological Survey on Alcohol and Related Conditions (NESARC), a nationally representative epidemiological study of alcohol, drug, and mental disorders in the United States, suggest that only about one-fourth of individuals with alcoholism have ever received treatment.
Thus, a substantial proportion of people with alcoholism were not represented in the samples previously used to define subtypes of this disease.
In the current study, Dr. Moss and colleagues applied advanced statistical methods to data from the NESARC. Their analyses focused on the 1,484 NESARC survey respondents who met diagnostic criteria for alcohol dependence, and included individuals in treatment as well as those not seeking treatment.
The researchers identified unique subtypes of alcoholism based on respondents’ family history of alcoholism, age of onset of regular drinking and alcohol problems, symptom patterns of alcohol dependence and abuse, and the presence of additional substance abuse and mental disorders:
Young Adult subtype: 31.5 percent of U.S. alcoholics. Young adult drinkers, with relatively low rates of co-occurring substance abuse and other mental disorders, a low rate of family alcoholism, and who rarely seek any kind of help for their drinking.
Young Antisocial subtype: 21 percent of U.S. alcoholics. Tend to be in their mid-twenties, had early onset of regular drinking, and alcohol problems. More than half come from families with alcoholism, and about half have a psychiatric diagnosis of Antisocial Personality Disorder. Many have major depression, bipolar disorder, and anxiety problems. More than 75 percent smoked cigarettes and marijuana, and many also had cocaine and opiate addictions. More than one-third of these alcoholics seek help for their drinking.
Functional subtype: 19.5 percent of U.S. alcoholics. Typically middle-aged, well-educated, with stable jobs and families. About one-third have a multigenerational family history of alcoholism, about one-quarter had major depressive illness sometime in their lives, and nearly 50 percent were smokers.
Intermediate Familial subtype: 19 percent of U.S. alcoholics. Middle-aged, with about 50 percent from families with multigenerational alcoholism. Almost half have had clinical depression, and 20 percent have had bipolar disorder. Most of these individuals smoked cigarettes, and nearly one in five had problems with cocaine and marijuana use. Only 25 percent ever sought treatment for their problem drinking.
Chronic Severe subtype: 9 percent of U.S. alcoholics. Comprised mostly of middle-aged individuals who had early onset of drinking and alcohol problems, with high rates of Antisocial Personality Disorder and criminality. Almost 80 percent come from families with multigenerational alcoholism. They have the highest rates of other psychiatric disorders including depression, bipolar disorder, and anxiety disorders as well as high rates of smoking, and marijuana, cocaine, and opiate dependence. Two-thirds of these alcoholics seek help for their drinking problems, making them the most prevalent type of alcoholic in treatment.
The authors also report that co-occurring psychiatric and other substance abuse problems are associated with severity of alcoholism and entering into treatment. Attending Alcoholics Anonymous and other 12-step programs is the most common form of help-seeking for drinking problems, but help-seeking remains relatively rare.

Source: National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism June 2007



]]> http://drugprevent.org.uk/ppp/2010/05/subtypes-of-alcoholism-discovered/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/the-new-science-of-neuroplasticity/ http://drugprevent.org.uk/ppp/2010/05/the-new-science-of-neuroplasticity/#comments Sat, 01 May 2010 11:08:01 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6506
For years, scientists described the human brain as a machine with parts, each part dedicated to controlling different activities. If a part was injured, the function it controlled would be lost permanently. But as Norman Doidge shows in his new book, The Brain That Changes Itself, (Viking) new neurological evidence has emerged showing that the brain can be trained to rewire itself after an injury, such as a stroke or ear or eye damage. Through interviews with neuroscientists and neuron-rehabilitation patients, Doidge also finds that the brain is capable of improving learning disabilities and intellectual and even moral performance through techniques such as repetition of learning and implementation of regular habits. The more we know about these processes, the more doctors can help patients to find other ways perform lost functions.

Doidge is a psychiatrist, psychoanalyst, and researcher on the research faculty at Columbia University’s Center for Psychoanalytic Training and Research, in New York, and the University of Toronto’s Department of Psychiatry.

Source: Hudson Institute August 2007



]]> http://drugprevent.org.uk/ppp/2010/05/the-new-science-of-neuroplasticity/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/nicotinic-receptors-may-be-important-targets-for-treatment-of-multiple-addictions/ http://drugprevent.org.uk/ppp/2010/05/nicotinic-receptors-may-be-important-targets-for-treatment-of-multiple-addictions/#comments Sat, 01 May 2010 11:07:08 +0000 ndpa http://drugprevent.org.uk/ppp/2010/05/nicotinic-receptors-may-be-important-targets-for-treatment-of-multiple-addictions/ For years, scientists have known that some people are biologically more susceptible to drug addiction than others, but they have only been able to speculate why.
In the August 15, 2007 issue of the Journal of Neuroscience, researchers at the University of Chicago report on a study that may help answer this question.
They discovered that rats most likely to self-administer addictive drugs had a particular receptor in the brain that is more responsive than the same receptor in rats least likely to self-administer addictive drugs.
This receptor, known as the nicotinic acetylcholine receptor (nAChR), increases excitability within in the brain’s reward centers. In the animals that were more likely to take addictive drugs, the effects of these receptors were much stronger, leading to more profound excitation of the cells and pathways associated with reward.
Stress, and the associated increases in stress hormones, will promote drug-taking behavior regardless of whether an animal is more or less susceptible, say the researchers. They showed that stress also increases the responses of nAChRs within the brain’s reward areas.
“We tested the exploratory behavior of rats in an unfamiliar cage. Rats that explore a new environment for a prolonged period of time were more interested in addictive drugs,” says Daniel McGehee, PhD, associate professor and lead researcher on this study. ” Those rats also had stronger nAChR responses, meaning their brains responded differently to the drugs. We measured receptor activity in the brain’s reward centers that are known to be activated by addictive drugs.”
“This study provides valuable insight into the mechanism of addiction,” says McGehee. “It raises the possibility that nicotinic receptors may be important targets for the treatment of multiple addictions, not just nicotine. Unfortunately, blocking these receptors may also interfere with healthy behaviors that depend upon the same brain circuitry. Precisely where these findings will lead drug treatment strategies is unclear, but this work provides insight into the role of nicotinic receptors in the vulnerability to multiple classes of addictive drugs.”

Source: University of Chicago Medical Center. Published on Eureka Alert August 2007



]]> http://drugprevent.org.uk/ppp/2010/05/nicotinic-receptors-may-be-important-targets-for-treatment-of-multiple-addictions/feed/ 0 http://drugprevent.org.uk/ppp/2010/05/brain-dysfunction-blamed-for-drug-fix/ http://drugprevent.org.uk/ppp/2010/05/brain-dysfunction-blamed-for-drug-fix/#comments Sat, 01 May 2010 11:05:08 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6502 Drug users who can’t kick the habit can blame a dysfunctional brain for their addiction, according to new research.
A study by the University of Melbourne has found long-term drug users have more difficulty controlling impulses because their frontal cortex is impaired.

The two-year study found opiate users needed to use more of their brains to resist impulses in a test of self control than those who were clean. The findings shed new light on why drug addicts find it so hard to quit, despite the health consequences.
“Drugs can capture and hijack some parts of the brain,” said Dr Murat Yucel, a lead researcher in the study. In this study we found the frontal cortex, an area that is essential for exercising control over thoughts and behaviours, was working inefficiently. These findings may help explain why it takes addicted individuals enormous effort to exercise control over their drug taking behaviour in the face of adverse consequences and why they are vulnerable to relapse back into uncontrolled, compulsive patterns of use.”
The study – published in the journal, Molecular Psychiatry, last month – also found drug users’ brain cells in the frontal region were less healthy than normal. The research shows drug taking is not a matter of choice for long-term users, who have a reduced biological capacity to stop, Dr Yucel says.
Researchers will next examine whether reduced brain function is a consequence of addiction or a contributing factor that makes some people more vulnerable to drug abuse. Co-researcher Dan Lubman said the study would likely lead to the development of new strategies for the treatment of addiction.
“These findings tell us that we need to provide a combination of pharmaceutical and psychological treatments that will help bolster the efficiency of the frontal cortex and hence the individual’s ability to stop their urge to use drugs,” he said.

Source: www.yahoo7News.com Aug. 2007



]]> http://drugprevent.org.uk/ppp/2010/05/brain-dysfunction-blamed-for-drug-fix/feed/ 0 http://drugprevent.org.uk/ppp/2010/04/strange-protein-in-brains-of-drug-users/ http://drugprevent.org.uk/ppp/2010/04/strange-protein-in-brains-of-drug-users/#comments Tue, 06 Apr 2010 20:22:28 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6426 September 7, 2007

Research Summary
Cocaine and amphetamine users appear to develop an abnormal protein in their brains that could play a role in addiction.
Researchers at the Rosalind Franklin University of Medicine and Science in North Chicago, Ill., found that use of these drugs alters a protein that controls how RNA is copied — an anomaly that could cause structural changes in tissues, diseases, and behavior changes.

Reference:
Marinescu V, Loomis PA, Ehmann S, Beales M, Potashkin JA (2007) Regulation of Retention of FosB Intron 4 by PTB. PLoS ONE, 2(9): e828; doi: 10.1371/journal.pone.0000828.
This article summarizes a mainstream media report of research published in a scientific journal. It is not an original analysis of the source material, which is cited in the reference above.

Source: online journal PLoS One. September 2007



]]> http://drugprevent.org.uk/ppp/2010/04/strange-protein-in-brains-of-drug-users/feed/ 0 http://drugprevent.org.uk/ppp/2010/04/drinking-alcohol-associated-with-smaller-brain-volume/ http://drugprevent.org.uk/ppp/2010/04/drinking-alcohol-associated-with-smaller-brain-volume/#comments Tue, 06 Apr 2010 20:17:44 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6416 Brain volume decreases with age at an estimated rate of 1.9 percent per decade, accompanied by an increase in white matter lesions, according to background information in the article. Lower brain volumes and larger white matter lesions also occur with the progression of dementia and problems with thinking, learning and memory. Moderate alcohol consumption has been associated with a lower risk of cardiovascular disease; because the brain receives blood from this system, researchers have hypothesized that small amounts of alcohol may also attenuate age-related declines in brain volume.
Carol Ann Paul, M.S., of Wellesley College, Mass., and colleagues studied 1,839 adults (average age 60) who were part of the Framingham Offspring Study, which began in 1971 and includes children of the original Framingham Heart Study participants and their spouses. Between 1999 and 2001, participants underwent magnetic resonance imaging (MRI) and a health examination. They reported the number of alcoholic drinks they consumed per week, along with their age, sex, education, height, body mass index and Framingham Stroke Risk Profile (which calculates stroke risk based on age, sex, blood pressure and other factors).
“Most participants reported low alcohol consumption, and men were more likely than women to be moderate or heavy drinkers,” the authors write. “There was a significant negative linear relationship between alcohol consumption and total cerebral brain volume.”
Although men were more likely to drink alcohol, the association between drinking and brain volume was stronger in women, they note. This could be due to biological factors, including women’s smaller size and greater susceptibility to alcohol’s effects.
“The public health effect of this study gives a clear message about the possible dangers of drinking alcohol,” the authors write. “Prospective longitudinal studies are needed to confirm these results as well as to determine whether there are any functional consequences associated with increasing alcohol consumption. This study suggests that, unlike the associations with cardiovascular disease, alcohol consumption does not have any protective effect on brain volume.”

Source: Paul et al. Association of Alcohol Consumption With Brain Volume in the Framingham Study. Archives of Neurology, 2008; 65 (10): 1363 DOI:


]]> http://drugprevent.org.uk/ppp/2010/04/drinking-alcohol-associated-with-smaller-brain-volume/feed/ 0 http://drugprevent.org.uk/ppp/2010/03/psychosis-more-common-among-teen-marijuana-users-study-2/ http://drugprevent.org.uk/ppp/2010/03/psychosis-more-common-among-teen-marijuana-users-study-2/#comments Tue, 16 Mar 2010 21:20:05 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6275 Smoking marijuana as a teenager could raise the risk of developing schizophrenia and psychotic symptoms as a young adult, according to a new study that compared the prevalence of mental illness among marijuana users and non-users.
Bloomberg News reported March 2 that researcher John McGrath of the University of Queensland, Australia, and colleagues studied 3,801 young-adult sibling pairs and concluded that those who used marijuana the longest (six or more years) were twice as likely to develop schizophrenia or delusional disorders. They also were four times more likely than non-users to score highly on a test gauging psychotic-like experiences.
Higher scores on the test also were seen among those who used marijuana for less than three years.

Source: www.jointogether.org March 2010

]]> http://drugprevent.org.uk/ppp/2010/03/psychosis-more-common-among-teen-marijuana-users-study-2/feed/ 0 http://drugprevent.org.uk/ppp/2010/03/genetic-risk-factors-for-both-marijuana-and-alcohol-misuse-similar/ http://drugprevent.org.uk/ppp/2010/03/genetic-risk-factors-for-both-marijuana-and-alcohol-misuse-similar/#comments Tue, 16 Mar 2010 21:19:01 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6273 • Marijuana is the most commonly used illicit drug in the United States.
• New research shows that the use and misuse of alcohol and marijuana are influenced by a common set of genes.
Marijuana is the most commonly used illicit drug in the United States. Roughly eight to 12 percent of marijuana users are considered “dependent” and, just like alcohol, the severity of symptoms increases with heavier use. A new study has found that use and misuse of alcohol and marijuana are influenced by a common set of genes.
Results will be published in the March 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
“Results from a large annual survey of high-school students show that in 2008, 41.8 percent of 12th graders reported having used marijuana,” explained Carolyn E. Sartor, a research instructor at Washington University School of Medicine and corresponding author for the study. “Although many may have used the drug on only a few occasions, 5.4 percent of 12th graders reported using it daily within the preceding month.”
“The active ingredient in marijuana is THC, which mimics natural cannabinoids that the brain produces,” added Christian Hopfer, associate professor at the University of Colorado School of Medicine. “The cannabinoid system is critical for learning, memory, appetite, and pain perception. Most users of marijuana will not develop an ‘addiction’ to it, but perhaps one in 12 will. What is not commonly appreciated about marijuana use is that strong evidence has emerged that it increases the risk of developing mental illnesses and possibly exacerbates pre-existing mental illnesses.”
“Like any drug, marijuana can be used in a way that negatively impacts quality of life, interfering with functioning at school or work or leading to problems with family and friends,” said Sartor. “Although at least three of six symptoms listed in the Diagnostic and Statistical Manual of Mental Disorders – Fourth Edition (DSM-IV) are needed to meet full criteria for cannabis (marijuana) dependence … the presence of even one or two of these symptoms could create distress or interfere with day-to-day functioning. There is strong evidence for a genetic component to use and dependence on marijuana as well as alcohol, and the use (and misuse) of these substances frequently occur together.”
Researchers examined 6,257 individuals (2,761 complete twin pairs and 735 singletons) listed in the Australian Twin Registry, 24 to 36 years of age. Alcohol and marijuana use histories were gathered in telephone diagnostic interviews and used to derive levels of alcohol consumption, frequency of marijuana use, and DSM-IV alcohol and cannabis dependence symptoms.
“Our findings indicate that … many of the same genetic factors that contribute to alcohol use also contribute to marijuana use,” said Sartor. “Likewise, alcohol dependence symptoms and cannabis dependence symptoms can be traced to some of the same genetic influences. For both alcohol and marijuana, the majority of genetic factors that contribute to use also contribute to dependence symptoms.”
“In other words,” said Hopfer, “the genetic influences on drug use are not specific to individual drugs, but seem to influence a general tendency to engage in drug use. This is important to note because there is a tendency to study drugs in isolation – alcohol, tobacco, marijuana, cocaine, etc. These findings add support to the notion of common mechanisms underlying all addictions.”
“The fact that very little of the environmental influences on alcohol and marijuana use, or on alcohol and cannabis dependence symptoms, could be traced to common sources indicates that there may be important distinctions between those environmental factors that influence alcohol-related outcomes and those that influence marijuana-related outcomes,” said Sartor. “Identifying alcohol- and marijuana-specific risk factors is an important next step in this line of research.”
“Marijuana research is relatively sparse compared to alcohol or nicotine research,” added Hopfer. “However, if you look at reports of at least adolescents and young people using, it becomes clear that marijuana use, including daily marijuana use, is quite common and the effects of this are not well understood. The mental illness/marijuana connection has not received much press, although I think the evidence has grown substantially that marijuana is a causal risk factor for the development of mental illness.”

Source: http://www.attcnetwork.org/explore/priorityareas/science/tools/asmeDetails.asp?ID=643

]]> http://drugprevent.org.uk/ppp/2010/03/genetic-risk-factors-for-both-marijuana-and-alcohol-misuse-similar/feed/ 0 http://drugprevent.org.uk/ppp/2010/03/more-evidence-of-marijuana-psychosis-link/ http://drugprevent.org.uk/ppp/2010/03/more-evidence-of-marijuana-psychosis-link/#comments Tue, 16 Mar 2010 21:17:24 +0000 ndpa http://drugprevent.org.uk/ppp/2010/03/more-evidence-of-marijuana-psychosis-link/  Marijuana use at a young age significantly increased the risk of psychosis in young adulthood, Australian investigators reported.

Young adults who reported a longer duration since first exposure to marijuana had a two- to fourfold greater prevalence of three different psychosis-related outcomes, John McGrath, MD, PhD, of the Queensland Center for Mental Health Research in Wacol, and colleagues concluded in an article published online in Archives of General Psychiatry.

Apart from the implications for policy makers and health planners, we hope our findings will encourage further clinical and animal model-based research to unravel the mechanisms linking cannabis use and psychosis, the researchers concluded.

Several prospective-cohort studies have demonstrated an association between early marijuana use and an increased risk of psychosis. On the basis of such studies, reviews of the issue have generally concluded that early use of marijuana, or cannabis, is a modifiable risk factor for psychosis-related outcomes, the authors wrote.

However, some concern has persisted about potential methodologic biases and unmeasured confounders in the cohort studies. In an effort to address the concern, McGrath and colleagues examined the association between cannabis use and psychosis in 3,800 participants in a long-term evaluation of pregnancy and outcomes. In contrast to prior cohort studies, the authors incorporated a subset analysis involving 228 sibling pairs.

“If a significant association between cannabis use and psychosis-related outcomes was not detected in sibling pairs, it would seriously weaken the argument that cannabis use was a risk-modifying factor for psychosis-related outcomes,” they wrote.

Participants were born between 1981 and 1984 at a single hospital in Brisbane. Mothers and their offspring were followed up at five, 14, and 21 years after birth. At the 21-year follow-up, McGrath and colleagues retrospectively assessed cannabis use among the offspring, whose age averaged 20 and ranged from 18 to 23.

Cannabis use was assessed by means of the young adults’ responses to two questions: In the last month, how often did you use cannabis, marijuana, pot, etc.? At what age did you first use cannabis?
Possible responses to the first question were never, every day, every few days, once or so, and not in the past month.

Investigators separated the cohort into four groups on the basis of self-reported cannabis use. One group included never-users, and the remaining three groups were categorized by duration since first use of cannabis: three years or less, four to five years, six years or more.

Investigators compared participants’ history of cannabis use with three psychosis-related outcomes: non-affective psychosis, hallucinations (assessed by the Computerized International Diagnostic Interview), and the Peters et al Delusions Inventory (PDI) score (Schizophr Bull 2004; 30: 1005-1022).

The authors found that 65 participants met criteria for a diagnosis of non-affective psychosis, and 233 reported at least one hallucination-related incident. The PDI has a score range of 0-21, and participants were grouped into PDI quartiles representing scores of =2, 3 or 4, 5 to 7, and =8.

The authors analyzed the results by means of two statistical models, one adjusted for participant sex and age at testing and the other adjusted for sex, age at testing, presence of hallucinations at the 14-year follow-up, and parental history of mental illness.

Using never-users as the reference, the odds ratio for non-affective psychosis increased from 1.5 to 2.1 or 2.2 in the two models as duration of first cannabis use increased. The odds for hallucinations increased from 1.4 to 2.5 and 1.5 to 2.8.

Comparing the lowest and highest quartiles of PDI scores, the authors found that the odds of a higher score increased from 1.6 to 4.0 or 4.3 as duration since first cannabis use increased.  Associations for all three psychosis-related outcomes were statistically significant in both models (P=0.001 to P<0.001).

The sibling analysis was limited to the PDI scores. For each pair, the authors calculated difference scores for duration since first cannabis use and PDI total score. The association between time since first cannabis use and PDI score remained statistically significant in the sibling subset analysis.

Limitations of the study included: retrospective self-reporting of time since first cannabis use, lack of data on cumulative exposure to cannabis, no clinical validation of non-affective psychosis diagnosis and lack of use of the instrument at the 14-year follow up, and loss of participants at the 21-year mark with significant differences in the group lost to follow up compared with those retained.

Source:. “Association between cannabis use and psychosis-related outcomes using sibling pair analysis in a cohort of young adults” Arch Gen Psychiatry 2010; DOI: 10.1001/archgenpsychiatry.2010.6.

]]> http://drugprevent.org.uk/ppp/2010/03/more-evidence-of-marijuana-psychosis-link/feed/ 0 http://drugprevent.org.uk/ppp/2010/03/research-triangle-international-%e2%80%93-a-prevention-science-approach/ http://drugprevent.org.uk/ppp/2010/03/research-triangle-international-%e2%80%93-a-prevention-science-approach/#comments Fri, 05 Mar 2010 13:51:14 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6190 My first appointment was with Dr Diana Fishbein, a Senior Fellow in behavioral neuroscience at the Research Triangle Institute (RTI) which is an international not-for-profit research organisation .

Diana is the Director of the Transdisciplinary Behavioural Science Program at RTI. In this role she focuses on bringing interdisciplinary teams of researchers together to try to answer some of the big questions that need to be asked in the behavioural sciences. Her overarching goal is to focus on the nexus between research and practice and to facilitate the “Translation of Research into Evidence Based Practice”. In fact RTI International organisational by line is Turning Knowledge into Practice.    

Diana’s personal research career has been in the area of criminology and drug abuse taking a prevention science approach.  She is particularly interested in why some young people respond well to a prevention approach while others don’t, and ultimately in determining “who responds to what treatment at what time point and why”?

To explore these questions she uses interdisciplinary methods and a developmental approach and sees the plasticity of neurobiological systems as one of the keys to finding the answer. Dr. Fishbein  pointed out that neuroplasticity enables neurobiological systems to be shaped by inputs from the environment and so can be altered for better or worse depending on the nature of these inputs. This is highly relevant to a prevention or early intervention approach and can guide the development of interventions. Research in this area is now beginning to focus on the mechanisms through which developmental risk factors impact on the developing systems and also on the type of interventions which have the most impact, how they are affecting neuroplastic change and when they are having the most effect.  

For instance there is evidence that the neurobiological functions underlying drug misuse and aggression are quite complex and include executive functioning, coping skills and affect regulation. The part of the brain associated with these functions (prefrontal-limbic brain networks) is not consolidated until early adulthood. Therefore is we can understand the type, effect and developmental timing of environmental impact on this brain function we may be able to plan intervention programs that alter negative impact and increase positive impact.  We may also need to tailor interventions to particular risk factors in the young person’s environment. Diana is confident this translational approach promises to eventually offer some direction for the design of effective interventions to prevent drug misuse and associated aggression.

This cutting-edge evidence-based research with the capacity to not only make a difference but to provide us with the scientific evidence to show how change has come about.  The message that again seems to be coming through to me is that one size is not likely to fit all. The other message is one that Professor Alan Hayes a member of the external advisory group for this project has written about in his chapter entitled Why early in life is not enough! (Hayes, 2007. In France, A & Homel, R (Eds) Pathways and crime prevention: Theory policies and practice  Willian (pps 202-225)

Dr Fishbein and I also talked about the need for parent and community involvement in interventions.  She also indicated to me that she and her organisation are very interested in innovative collaborative international research. Perhaps this is something to think about for the future.

Source: http://shapingbrains.wordpress.com  3^rd March 2010

 

 

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]]> http://drugprevent.org.uk/ppp/2010/03/research-triangle-international-%e2%80%93-a-prevention-science-approach/feed/ 0 http://drugprevent.org.uk/ppp/2010/03/recreational-cocaine-use-may-impair-inhibitory-control/ http://drugprevent.org.uk/ppp/2010/03/recreational-cocaine-use-may-impair-inhibitory-control/#comments Wed, 03 Mar 2010 21:23:13 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6137 The recreational use of cocaine has rapidly increased in many European countries over the past few years. One cause of this is the fall in the price of the drug on the street from 100 Euros for one gram (about 5 lines) in 2000 to 50 Euros in the Netherlands today. One line of cocaine is, thus, now as cheap as a tablet of ecstasy. This means cocaine is no longer considered an “elite” drug but is affordable for all, especially for recreational use. It is therefore likely that the recreational use of cocaine will become a public health issue in the next few years, which is already the case for the recreational use of ecstasy.
In a study in PLoS One, researchers at Leiden University and the University of Amsterdam, led by Lorenza Colzato, employed the “stop-signal paradigm” to measure the length of time taken by subjects to initiate and suppress a prepared reaction.
The stop-signal task requires participants to react quickly and accurately by pressing a left or right key in response to the direction of a left- or right-pointing green arrow. In 30% of the trials, the green arrow turned red, in which case participants had to abort the go response. The results show that while both recreational users of cocaine and non-users performed similarly in terms of response initiation, users needed significantly more time to inhibit their responses.
The study is the first of its kind to investigate systematically action control, and the inhibitory control of unwanted response tendencies in particular, in recreational users, i.e. those who don’t meet the criteria for abuse or dependency but who take cocaine (usually by snorting) on a monthly basis (1 to 4 grams). The researchers found that the magnitude of the inhibitory deficit in recreational users was smaller than previously observed in chronic users, suggesting that the degree of the impairment is proportional to the level of cocaine use.
Given the seemingly small quantities of cocaine involved, the findings of this study are rather worrying. Many real-life situations require the active inhibition of pre-potent actions, as in the case of traffic lights turning red or of criminal actions. This impairment of inhibitory control has serious implications for personal or societal functioning. This reduced level of inhibitory control may even be involved in the emergence of addiction: the more a drug is used, the less able users are to prevent themselves from using it.

Source: Public Library of Science PLoS One 2(11): e1143.doi:10.1371/journal.pone.0001143 2007, November 7.

]]> http://drugprevent.org.uk/ppp/2010/03/recreational-cocaine-use-may-impair-inhibitory-control/feed/ 0 http://drugprevent.org.uk/ppp/2010/03/ecstasy-can-harm-the-brains-of-first-time-users/ http://drugprevent.org.uk/ppp/2010/03/ecstasy-can-harm-the-brains-of-first-time-users/#comments Wed, 03 Mar 2010 21:22:35 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6135 Researchers have discovered that even a small amount of MDMA, better known as ecstasy, can be harmful to the brain, according to the first study to look at the neurotoxic effects of low doses of the recreational drug in new ecstasy users. The findings were presented today at the annual meeting of the Radiological Society of North America (RSNA).

“We found a decrease in blood circulation in some areas of the brain in young adults who just started to use ecstasy,” said Maartje de Win, M.D., radiology resident at the Academic Medical Center at the University of Amsterdam in the Netherlands. “In addition, we found a relative decrease in verbal memory performance in ecstasy users compared to non-users.”
Ecstasy is an illegal drug that acts as a stimulant and psychedelic. A 2004 survey by the National Institute on Drug Abuse (NIDA) found that 450,000 people in the United States age 12 and over had used ecstasy in the past 30 days. In 2005, NIDA estimated that 5.4 percent of all American 12th graders had taken the drug at least once.
Ecstasy targets neurons in the brain that use the chemical serotonin to communicate. Serotonin plays an important role in regulating a number of mental processes including mood and memory.
Research has shown that long-term or heavy ecstasy use can damage these neurons and cause depression, anxiety, confusion, difficulty sleeping and decrease in memory. However, no previous studies have looked at the effects of low doses of the drug on first-time users.
Dr. de Win and colleagues examined 188 volunteers with no history of ecstasy use but at high-risk for first-time ecstasy use in the near future. The examinations included neuroimaging techniques to measure the integrity of cells and blood flow in different areas of the brain and various psychological tests. After 18 months, 59 first-time ecstasy users who had taken six tablets on average and 56 non-users were re-examined with the same techniques and tests.
The study found that low doses of ecstasy did not severely damage the serotonergic neurons or affect mood. However, there were indications of subtle changes in cell architecture and decreased blood flow in some brain regions, suggesting prolonged effects from the drug, including some cell damage. In addition, the results showed a decrease in verbal memory performance among low-dose ecstasy users compared to non-users.
“We do not know if these effects are transient or permanent,” Dr. de Win said. “Therefore, we cannot conclude that ecstasy, even in small doses, is safe for the brain, and people should be informed of this risk.”
This research is part of the Netherlands XTC Toxicity (NeXT) study, which also looks at high-dose ecstasy users and aims to provide information on long-term effects of ecstasy use in the general population.

Source: Radiological Society of North America (2006, November 28).

]]> http://drugprevent.org.uk/ppp/2010/03/ecstasy-can-harm-the-brains-of-first-time-users/feed/ 0 http://drugprevent.org.uk/ppp/2010/03/teens-smoking-marijuana-at-increased-schizophrenia-risk/ http://drugprevent.org.uk/ppp/2010/03/teens-smoking-marijuana-at-increased-schizophrenia-risk/#comments Wed, 03 Mar 2010 21:20:29 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6129 Teens who smoke marijuana are at a greater risk of developing schizophrenia and psychotic symptoms in the future, a new study has found.
After observing more than 3800 youngsters, researchers learnt that people who used the drug for six or more years were twice as likely to suffer from delusional disorders than those who never used it. Researchers from Queensland Brain Institute, at the University of Queensland, quizzed 3801 young adults who were born in Brisbane between 1981 and 1984.
Among the 1272 participants who had never used marijuana, 26 (2 per cent) were diagnosed with psychosis, while the 322 people who had used marijuana for six or more years, 12 (3.7 per cent) were diagnosed with the illness. The average age of the participants was about 20. According to the authors, the study was the first to look at sibling pairs to discount genetic or environmental influence.
“This is the most convincing evidence yet that the earlier you use cannabis, the more likely you are to have symptoms of a psychotic illness,” the Sydney Morning Herald quoted Dr McGrath, a professor at the institute, as saying in a statement.
McGrath added: “The message for teenagers is: if they choose to use cannabis they have to understand there’s a risk involved.” The study noted: “Apart from the implications for policy makers and health planners, we hope our findings will encourage further clinical and animal-model research to unravel the mechanisms linking cannabis use and psychosis.”
The research has been published online by the Archives of General Psychiatry.

Source: Health Wise Feb 28 2009

]]> http://drugprevent.org.uk/ppp/2010/03/teens-smoking-marijuana-at-increased-schizophrenia-risk/feed/ 0 http://drugprevent.org.uk/ppp/2010/03/heavy-marijuana-use-damages-young-minds/ http://drugprevent.org.uk/ppp/2010/03/heavy-marijuana-use-damages-young-minds/#comments Wed, 03 Mar 2010 21:17:34 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6121 Teens and young adults who are heavy marijuana users are more likely than non-users to have disrupted brain development, according to a new study that appeared last month in the Journal of Psychiatric Research.

Pediatric researchers found abnormalities in areas of the brain that interconnect regions involved in memory, attention, decision-making, language and executive functioning skills. The findings are of particular concern because adolescence is a crucial period for brain development and maturation.

The researchers caution the study is preliminary and does not demonstrate that marijuana use causes the brain abnormalities. However, “Studies of normal brain development reveal critical areas of the brain that develop during late adolescence, and our study shows that heavy cannabis use is associated with damage in those brain regions,” said study leader Manzar Ashtari, Ph.D., director of the Diffusion Image Analysis and Brain Morphometry Laboratory in the Radiology Department of The Children’s Hospital of Philadelphia.

Working with child psychiatrist Sanjiv Kumra, M.D., Ashtari and colleagues performed imaging studies on 14 young men from a residential drug treatment center in New York, as well as 14 age-matched healthy controls. All the study subjects were males, with an average age of 19. The researchers performed the imaging studies at Long Island Jewish Medical Center.

The 14 subjects from the drug treatment center all had a history of heavy cannabis use during adolescence. Most had smoked marijuana from age 13 till age 18 or 19, and reported smoking nearly six marijuana joints daily in the final year before they stopped using the drug.

The study team performed a type of magnetic resonance imaging scan called diffusion tensor imaging (DTI) that measures water movement through brain tissues. The abnormal patterns of water diffusion that were found among the young adults with histories of marijuana use suggest damage or an arrest in development of the myelin sheath that surrounds brain cells, Ashtari said. Myelin provides a coating around brain cells similar to insulation covering an electrical wire. If myelin does not function properly, signaling within the brain may be slower.

Myelin gives its color to the white matter of the brain, and covers the nerve fibers that connect different brain regions. The study’s results suggest early-onset substance use may alter the development of white matter circuits, especially those connections among the frontal, parietal and temporal regions of the brain. Abnormal white matter development could slow information transfer in the brain and affect cognitive functions

Source: the Journal of Psychiatric Research. Reported in CADCA Coalitions online Feb 24 2010

]]> http://drugprevent.org.uk/ppp/2010/03/heavy-marijuana-use-damages-young-minds/feed/ 0 http://drugprevent.org.uk/ppp/2010/03/everyday-and-prospective-memory-deficits-in-ecstasypolydrug-users/ http://drugprevent.org.uk/ppp/2010/03/everyday-and-prospective-memory-deficits-in-ecstasypolydrug-users/#comments Wed, 03 Mar 2010 21:16:41 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6119
Abstract
The impact of ecstasy/polydrug use on real-world memory (i.e. everyday memory, cognitive failures and prospective memory [PM]) was investigated in a
sample of 42 ecstasy/polydrug users and 31 non-ecstasy users. Laboratory-based PM tasks were administered along with self-reported measures of PM to
test whether any ecstasy/polydrug-related impairment on the different aspects of PM was present. Self-reported measures of everyday memory and
cognitive failures were also administered. Ecstasy/polydrug associated deficits were observed on both laboratory and self-reported measures of PM and
everyday memory. The present study extends previous research by demonstrating that deficits in PM are real and cannot be simply attributed to
self-misperceptions. The deficits observed reflect some general capacity underpinning both time- and event-based PM contexts and are not task
specific. Among this group of ecstasy/polydrug users recreational use of cocaine was also prominently associated with PM deficits. Further research
might explore the differential effects of individual illicit drugs on real-world memory.

Source: Journal of Psychopharmacology 0(00) 1–12 2010


]]> http://drugprevent.org.uk/ppp/2010/03/everyday-and-prospective-memory-deficits-in-ecstasypolydrug-users/feed/ 0 http://drugprevent.org.uk/ppp/2010/02/cannabis-use-and-risk-of-psychotic-or-affective-mental-health/ http://drugprevent.org.uk/ppp/2010/02/cannabis-use-and-risk-of-psychotic-or-affective-mental-health/#comments Fri, 12 Feb 2010 21:31:49 +0000 ndpa http://drugprevent.org.uk/ppp/?p=6074
Theresa H M Moore, Stanley Zammit, Anne Lingford-Hughes, Thomas R E Barnes, Peter B Jones, Margaret Burke, Glyn Lewis
Summary
Background – Whether cannabis can cause psychotic or affective symptoms that persist beyond transient intoxication is unclear. We systematically reviewed the evidence pertaining to cannabis use and occurrence of psychotic or affective mental health outcomes.
Methods – We searched Medline, Embase, CINAHL, PsycINFO, ISI Web of Knowledge, ISI Proceedings, ZETOC, BIOSIS, LILACS, and MEDCARIB from their inception to September, 2006, searched reference lists of studies selected for inclusion, and contacted experts. Studies were included if longitudinal and population based. 35 studies from 4804 references were included. Data extraction and quality assessment were done independently and in duplicate.
Findings – There was an increased risk of any psychotic outcome in individuals who had ever used cannabis (pooled adjusted odds ratio=1•41, 95% CI 1•20–1•65). Findings were consistent with a dose-response eff ect, with greater risk in people who used cannabis most frequently (2•09, 1•54–2•84). Results of analyses restricted to studies of more clinically relevant psychotic disorders were similar. Depression, suicidal thoughts, and anxiety outcomes were examined separately.
Findings for these outcomes were less consistent, and fewer attempts were made to address non-causal explanations, than for psychosis. A substantial confounding eff ect was present for both psychotic and aff ective outcomes.
Interpretation The evidence is consistent with the view that cannabis increases risk of psychotic outcomes independently of confounding and transient intoxication eff ects, although evidence for aff ective outcomes is less strong. The uncertainty about whether cannabis causes psychosis is unlikely to be resolved by further longitudinal studies such as those reviewed here. However, we conclude that there is now suffi cient evidence to warn young people that using cannabis could increase their risk of developing a psychotic illness later in life.

Source: The Lancet Vol.370 pp 319-328 July 2007

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