TORONTO, Nov. 2 — Methamphetamine can be detected in the hair of newborns whose mothers used the drug during pregnancy, researchers here have found.
Action Points

• Note that this study shows that methamphetamine used during pregnancy can be found in the hair of neonates, suggesting it crosses the placental barrier with effects that are not completely understood.
• Advise patients who ask that drug abuse during pregnancy can be detrimental to the fetus, with a range of physical and intellectual sequelae, as well as hazardous to the mother.

It represents the first direct evidence in humans that crystal meth, which is a growing drug-abuse problem in North America, can cross the placenta and affect the growing fetus, according to Facundo Garcia-Bournissen, M.D., of the Motherisk program at the Hospital for Sick Children.
Researchers at the program have been testing hair samples from parents and adults across Canada for several years, usually when there is clinical suspicion of drug abuse on the part of parents, Dr. Garcia-Bournissen and colleagues reported in the online issue of Archives of Disease in Childhood.
From June 1997 through December 2005, the database accumulated results of 34,278 tests for drugs in hair, representing 8,270 people. Nearly 60% (or 4,926) of these people were positive for at least one drug of abuse, the researchers said.
In a retrospective analysis, Dr. Garcia-Bournissen and colleagues examined the incidence of methamphetamine in hair samples:

• The first methamphetamine was found in hair in 2003, when six samples tested positive, with a slight increase in 2004, with eight cases.
• There were 372 cases in 2005 and the researchers said preliminary data for 2006 indicates that the surge has not stopped.
• The study identified 11 mother-neonate pairs in which each was positive for methamphetamine.
• Also, one newborn was negative, although the mother was positive.

The median methamphetamine values in the mother-baby pairs were 1.75 ng/mg for the mothers and 1.63 ng/mg for the newborns. Dr. Garcia-Bournissen and colleagues said. The median concentrations were not significantly different, “suggesting that the transplacental transfer of methamphetamine is extensive,” the researchers said. On an individual level, maternal and neonatal drug levels correlated significantly (at P=0.003, using Spearman’s rho test, with r=0.8).
Interestingly, among the 171 subjects who were positive for methamphetamine and whose hair was tested for other drugs, 83.5% were positive for at least one other drug, usually cocaine, Dr. Garcia-Bournissen and colleagues found.
In contrast, among the 1,053 subjects negative for methamphetamine but positive for some other drug, only 38% were positive for more than one drug, they said.
“Positive exposure to methamphetamine strongly suggests that the person is a polydrug user, which may have important implications for fetal safety,” the researchers said. The effects of the drug on the exposed child remain unclear, Dr. Garcia-Bournissen and colleagues noted, although there is some evidence that “children exposed in utero to methamphetamine are at risk of developmental problems, because of either the effect of direct exposure to the drug during pregnancy or growing in the environment associated with parental methamphetamine misuse, or probably both.”

Because the study was retrospective and anonymous, clinical information on the exposed infants is not available, the researchers said.

Source: www.medpage.today.com 2nd Nov. 2006

Using an integrative meta-analysis approach, researchers from the Center for Bioinformatics at Peking University in Beijing have assembled the most comprehensive gene atlas underlying drug addiction and identified five molecular pathways common to four different addictive drugs. This novel paper appears in PLoS Computational Biology on January 4, 2008.
Drug addiction is a serious worldwide problem with strong genetic and environmental influences. So far different technologies have revealed a variety of genes and biological processes underlying addiction. However, individual technology can be biased and render only an incomplete picture. Studying individual or a small number of genes is like looking at pieces of a jigsaw puzzle – only when you gather most of the pieces from different places and arrange them together in an orderly fashion do interesting patterns emerge.
The team, led by Liping Wei, surveyed scientific literature published in the past 30 years and collected 2,343 items of evidence linking genes and chromosome regions to addiction based on single-gene strategies, microarray, proteomics, or genetic studies. They made this gene atlas freely available in the first online molecular database for addiction, named KARG (http://karg.cbi.pku.edu.cn), with extensive annotations and friendly web interface.
Assembling the pieces of evidence together, the authors identified 18 molecular pathways that are statistically enriched in the addiction-related genes. They then identified five pathways that are common to addiction to four different substances. These common pathways may underlie shared rewarding and response mechanisms and may be targets for effective treatments for a wide range of addictive disorders.

Source:News-Medical.net 7th Jan.2008  http://www.plos.org/

Chronic cannabis abuse raises nerve growth factor serum concentrations in drug-naive schizophrenic patients
Maria C. Jockers-Schertibi, Uta Matthies. Heidi Danker-Hopfe, Undine E. Lang Richard
Ivlahlberg and Rainer heliweg  Department of Psychiatry and Psychotherapy, Char ftc-University Medicine Berlin Campus Benjamin F,thjkiin. Berth,. German
Long-term cannabis abuse may increase the risk of schizophrenia. Nerve growth factor (NGF) is a pleiotropic neurotrophic protein that is implicated in development, protection and regeneration of NFG sensitive neurones. We tested the hypothesis that damage to neuronal cells in schizophrenia is precipitated by the consumption of cannabis and other neurotoxic substances, resulting in raised NGF serum concentrations and a younger age for disease onset.

The NGF serum levels of 109 consecutive drug-naive schizophrenic patients were measured and compared with those of healthy controls. The results were correlated with the long-term intake of cannabis and other illegal drugs. Mean (± SD) NGF serum levels of 61 control persons (33.1 ± 31.0 pg and 76 schizophrenics who did not consume illegal drugs (26.3 ± 19.5 pg/mi) did not differ significantly, Schizophrenic patients with regular cannabis intake (> 0.5 g on average per day for at least 2 years) had significantly raised NGF serum levels of 412.9 ± 288.4 pg/mI Cu 21) compared to controls and schizophrenic patients not consuming cannabis (p c 0001). In schizophrenic patients who abused not only cannabis, but also additional substances, NGF concentrations were as high as 2336.2 ± 1711.4 pg C = 12).

On average, heavy cannabis consumers suffered their first episode of schizophrenia 3.5 years (n = 21) earlier than schizophrenic patients who abstained from cannabis. These results indicate that cannabis is a possible risk factor for the development of schizophrenia. This might be reflected in the raised NGF-serum concentrations when both schizophrenia and long-term cannabis abuse prevail.
Discussion
These results demonstrate that serum NOF concentrations in untreated schizophrenic patients differed greatly depending on their long-term intake of drugs of abuse. Whereas he drug-naive schizophrenic patients who had not consumed illegal substances n the past showed no significant difference in senim NGF concentrations, those abusing cannabis for longer than 2 years showed significantly elevated N compared to healthy controls. This has been shown unequivocally not only by a descriptional data analysis, but also by a confirmatory study design (Table 2). Schizophrenic patients with long-term abuse of multiple substances showed an even greater increase in their serum NGF concentrations up to 90-fold above non-abusing schizophrenic patients (Fig. I).
NGF-plasma levels in 26 male schizophrenic patients who had been kept free of neuroleptics for 14 days were reported to be significantly lower than those observed in controls (Bersani er a!., 1999 By contrast, in our much larger sample of patients, we found no significant differences with respect to senim NGF concentrations between schizophrenic patients and controls. However, our patients were completely drug-naive whereas the patients of the formerly cited study previously had been treated with antipsvchotics for various time spans. It is known that haloperidol can remain in the cerebral tissue for as long as year after application (Konihuber et at, 1999) thereby possibly modulating and influencing NGF values by its antidopaminergic properties. For this reason, a drug-free period of l days might be too short to rule out the pharmacologica effects of footer antipsychotic medication on the NOF concentration. Haloperidol reduces the basal tTGF plasma levels in eight formerly neuroleptic’ free schizophrenic patients (ALoe et at. 1997).

One explanation could he co-secretion of ‘1GF with prolactin. with both being control by activation of the dopamine D: receptor subtype Missale er a!.. L 996) that, in turn, can be blocked by the antidopamine drug haloperidol. Moreover brain-derived neurotrophic factor (BDNF). another NGF-related neurotrophin. was 1-cc shown to be decreased in he serum of chronic schizophrenic patients who were already treated with neuroleptics Tovooka ci at. 2002). However. we demonstrated highly signficant elevations of the NOF serum levels in schizophrenic patients who had consumed significant amounts of cannabis in the past i more than 0.5 per day over at least 2 years). There’s strong circumstantial evidence for neuronal damage by toxic drugs, but only a few ( neurochenhical) studies to support this. Schizophrenia. a disease of alleged neurodevelopmental origin. o begins in M. C. JOCKERS-SCHERCJBL ETAL.: SCHIZOPHRENIA! CANNABIS AND NERVE GROWTH FACTOR 443 1 I
adolescence at age 6—24 years and is thought to coincide with increased vulnerability to cannabinoids. sometimes avert triggered by them (Andreasson era!.. 1987: Linszen eta!.. 994). In analogy to the situation in neurodegenerative disease (for reviews, see Heliweg et a!, 1998; Siegel and Chauhan, 2000). the high levels of NOF observed in our study might reflect the assumed adverse effects induced by cannabis consumption in schizophrenia development.
At present, the causes and mechanisms of the observed rise in NGF serum concentrations in schizophrenia following long-term cannabis abuse remain speculative. Similarly, from the present data, it is not possible to establish whether the rise in NGE levels is due to disease development (enhanced by cannabis) as a stale marker or whether NOF was even already high before disease onset. Theoretically, patients at risk for an unfavourable outcome of schizophrenia due to repeated cannabis consumption could be assumed to be a different patient population altogether and show premorbid rises in NOF concentrations as a risk-trait variable. 1 a small sample (n = I of subjects without schizophrenia, but regular cannabis consumption of at least 0.5 g per day for longer than 2 years. we found no such elevation of NOF measurements in the serum.

The same was true when serum NGF concentrations were measured in otherwise healthy controls acutely intoxicated with cannabis ( 5; Anders and He unpublished data), These findings indicate that the rise in NOF concentrations is not an effect of chronic cannabis consumption per Se but rather reflects the combined damaging effects of cerebral vulnerability in schizophrenia and the chronic toxicity of long-term cannabis abuse. The earlier onset of schizophrenia in the cannabis consuming patients (Table I) further substantiates this hypothesis.
Greatly raised NGF serum concentrations have been demon strated hi chronic diseases such as alcohol dependence (Aloe a at.. 1996) or Behcet’s disease (lockers-Scherlibi C a 1996). They are not specific for a certain diagnosis. but rather are a marker for chronicity of disease, and possibly for poor prognosis as seen in Behcet’s disease.

Our finding of even greater serum NOF concen [ in schizophrenic patients with a long-terni consumption of additional substances with neurotoxic effects is consistent with the hypothesis of an NOF correlation with the cumulative dose and toxicity of drugs. The rise was up to 90-fold of the mean NGF serum concentrations of schizophrenic patients without drug consumption, which corresponds to the highest endogenous TGF concentrations reported for man to date. Accordingly, cumulative doses of ecstasy have been demonstrated to be neurotoxic and exert delayed and/or chronic cerebral alterations (Ricaurte and \lcCann. 992). showing altered glucose metabolism in Positron emission tomography studies in the hippocampus and amygdala of seven chronic ecstasy users (Obrocki er a,. 1999). Previous magnetic resonance imaging studies with chronic drug abusers of various drugs including cocaine, amphetamines and psvchedelics. also showed minor structural brain changes (Aasley et at.. 1993). However, the investigators did note that the study probands had also been consuming alcohol, Therefore, the structural central nervous system changes did not clearly reflect those effects exclusively attributable to illegal drugs, but possibly also those due at least in part to alcohol. To avoid such confounding factors in our study, we excluded those patients who consumed alcohol on a re basis, This explains the lack of a control group with polysubstance abuse but no schizophrenia because we were unable to find probands that were otherwise reasonably healthy and consumed no alcohol. Certainly, this remains a field for future resarch.
The origin of the NOF measured in serum is speculative: On the one hand, serum NGF could well stem from a central source and reflect the central neurotrophin state, especially in pathological conditions such as preclinical Alzheimer’s disease (Schaub er a!.. 2002). On the other hand, it could reflect a peripheral immunological reaction in terms of a cytokine released from peripheral immune cells (for reviews, see Levi-Montalcini el c 1996; Hel er a.. 1998). Schizophrenia has been connected to autoimmune disease (Ganguli er aI.. 1994; Jones and Cannon. 1998) and to inflammatory disease (Lin eLa!.. 199B). both possibly resulting in central or peripheral immune responses.

An argument could be made about the principal evidence for a role of the neurotrophins NOF or BDNF in conjunction with schizophrenia. In the meantime, there are a number of experiments indicating a connection between BDNF and schizophrenia (Toyooka et at 2002) and some indicating NOF as not only having a role as a peripheral cytokine. but also as a factor relevant to schizophrenia (for a review, see Aloe et ci., 2000).
In summary, we suggest that the raised NOF serum concentrations found in schizophrenics with long-term cannabis abuse, and more so in schizophrenics with long-term abuse of additional drugs, reflect the amount of cerebra! damage by the combined effects of a primary cerebral vulnerability resulting from schizophrenia and the supposed additional drug-neurotoxicity. Apart from the biochemical evidence of an additive effect of schizophrenia and cannabis consumption on NGF serum concen ations in our confirmatory study design, we also demonstrated an earlier ons of disease in schizophrenic patients consuming cannabis chronically, thereby underlining a precipitating effect of the drug on disease onset. Those two findings am suggestive of a correlation but further studies are required to confirm this hypo thesis. Thus, cannabis use may be a risk factor in schizophrenia development, but a predisposition to schizophrenia and cannabis use combined (but neither one independently) appears to be linked to increased NOR production.
Acknowledgement
We would like to thank Dr Hans Scherubl manuscript and giving valuable advice.

Source:
Journal of Psychopharmacology 17(4) (2 439—445
V2003 British Aisociatlon For Psychopharmacology (ISSN Oz I
SAGE PublicaUons. London. Thousand Oaks. CA and Naw Delhi
0269—08111200312117:4: 439—445; O38O3

The percentage of fatally injured drivers testing positive for drugs increased over the last five years, according to data from the National Highway Traffic Safety Administration (NHTSA). Each year between 56% and 65% of drivers fatally injured in motor vehicle crashes were tested for the presence of drugs in their systems.

In 2009, 33% of the 12,055 of drivers fatally injured in motor vehicle crashes with known test results tested positive* for at least one drug, compared to 28% in 2005 (see figure below). The drugs tested for included both illegal substances as well as over-the counter and prescription medications, (which may or may not have been misused). In 2009, marijuana was the most prevalent drug found in this population—approximately 28% of fatally injured drivers who tested positive were positive for marijuana. The authors caution that “drug involvement rates among those with unavailable drug test results may be similar to those for whom results are available, or there may be a systematic bias that could influence the unavailable rates in a positive or negative direction.”

*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

Vol. 13, Issue 26
Distribution: 6,606
U n i v e r s i t y o f M a r y l a n d , C o l l e g e P a r k

A Weekly FAX from the Center for Substance Abuse Research
Nine behaviors and attitudes differentiate students who used marijuana before age 15 from those who had not, according to an analysis of data from the 2002 Maryland Adolescent Survey (MAS). Overall, one-fifth of Maryland12th grade students reported using marijuana before age 15.

A scale of 9 warning signs of early marijuana use among 12th graders was developed from an analysis of the MAS data (see below). The scale also detected early use among 8th and 10th graders. The more warning signs a student had, the more likely he or she was to have used marijuana early (see Figure 1). For example, approximately three-fourths of 12th graders with 6 or more warning signs were early marijuana users, compared to 3% of 12th graders with no warning signs.
Students with more warning signs also reported using a greater number of other illegal drugs* and experiencing a greater number of serious problems resulting from drug and alcohol use (see Figure 2). The report, “Warning Signs for Early Marijuana Users Among Maryland’s Public School Students,” discusses the implications of these findings for intervening with youth and implementing prevention programs. Complimentary copies of the report can be ordered by contacting CESAR at cesar@cesar.umd.edu or 301-405-9770.

The 9 Warning Signs for Early Marijuana Use:

Alcohol & Drug Problems Other Illegal Drugs Used
Figure 1: Percentage of Maryland
12th Grade Students Reporting
Marijuana Use Before Age 15

*Other illegal drugs were inhalants, nitrates, crack, cocaine, LSD, PCP, other hallucinogens, methamphetamines, designer drugs, heroin, amphetamines,
barbiturates, narcotics, and Ritalin®.

Figure 2: Mean Number of Other Illegal Drugs* Used
in Lifetime and Alcohol and Drug Problems**
by Maryland 12th Graders

**Alcohol and drug problems were school absences, health problems, family problems, being high/drunk at school, poor school performance, inability to stop
using drugs/alcohol, and driving while under the influence of alcohol/drugs.
301-405-9770 (voice) 301-403-8342 (fax) CESAR@cesar.umd.edu www.cesar.umd.edu

CESAR FAX is supported by BYRN 2003-1006, awarded by the U.S. Department of Justice through the Governor’s Office of Crime Control and Prevention.

SOURCE: Maryland Drug Early Warning System (DEWS), CESAR, “Warning Signs for Early Marijuana Users Among Maryland’s Public School Students,” DEWS Investigates, June 2004. For more information, contact Dr. Eric Wish at ewish@cesar.umd.edu.

Source: CesarFax June 28, 2004

This week, The National Center on Addiction and Substance Abuse at Columbia University released the National Survey of American Attitudes on Substance Abuse XVI: Teens and Parents. This year’s survey reveals that teens who regularly use social networking sites are at increased risk of smoking, drinking and using drugs. The survey finds that compared to teens who in a typical day do not spend any time on a social networking site, those who do are five times likelier to use tobacco, three times likelier to use alcohol, and twice as likely to use marijuana.

The CASA Columbia survey also reveals that 40 percent of all teens surveyed have seen pictures on Facebook, Myspace or other social networking sites of kids getting drunk, passed out, or using drugs and kids who have seen such pictures at also at increased substance abuse risk.

This year’s survey explored teen TV viewing habits in relation to teen substance abuse and found that compared to teens that do not watch suggestive teen programming, those who do are likelier to smoke, drink and use drugs.

According to Joseph A. Califano, Jr., CASA Columbia’s Founder and Chairman and Former U.S. Secretary for Health, Education, and Welfare: “The relationship of social networking site images of kids drunk, passed out, or using drugs and of suggestive teen programming to increased teen risk of substance abuse offers grotesque confirmation of the adage that a picture is worth a thousand words. The time has come for those who operate and profit from social networking sites like Facebook to deploy their technological expertise to curb such images and to deny use of their sites to children and teens who post pictures of themselves and their friends drunk, passed out or using drugs. Continuing to provide the electronic vehicle for transmitting such images constitutes electronic child abuse.”
Source: www.CADCA.org Aug. 2011

BRIAN DONNELLY

THE controversial heroin substitute methadone was implicated in more deaths than the drug itself in two areas of Scotland last year.
The figures for the Lothians show methadone was implicated in 33 deaths, while the comparable figure for heroin was 26. In Grampian, another historical centre of drug abuse, the substitute was a factor in 19 deaths, set against 14 for heroin.
The Scottish Drugs Forum (SDF), the national non- government drugs policy and information agency, said the prevalence of the substitute was “concerning”, while Tory health spokesman Murdo Fraser MSP said the figures showed there was a clear breakdown in the support system.

Source: www.Herald Scotland.com 17th Aug. 2011

ABSTRACT

The most extensive study of drug courts—a five-year examination of 23 courts and six comparison jurisdictions in eight states—found that these court programs can significantly decrease drug use and criminal behavior, with positive outcomes ramping upward as participants sensed their judge treated them more fairly, showed greater respect and interest in them, and gave them more chances to talk during courtroom proceedings.
WASHINGTON, D.C., July 18, 2011—Proponents of the adage that one person can change the world need look no farther than the country’s nearly 1,400 adult drug courts, which couple substance-abuse treatment with close judicial supervision in lieu of incarceration.
The most extensive study of drug courts—a five-year examination of 23 courts and six comparison jurisdictions in eight states—found that these court programs can significantly decrease drug use and criminal behavior, with positive outcomes ramping upward as participants sensed their judge treated them more fairly, showed greater respect and interest in them, and gave them more chances to talk during courtroom proceedings.
“Judges are central to the goals of reducing crime and substance use. Judges who spend time with participants, support them, and treat them with respect are the ones who get results,” said the Urban Institute’s Shelli Rossman, who led the research team from the Institute’s Justice Policy Center, the Center for Court Innovation, and RTI International.
Drug court participants who had more status hearings with the judge and received more praise from the judge later reported committing fewer crimes and using drugs less often than those who had less contact and praise. Court programs whose judges exhibited the most respectfulness, fairness, enthusiasm, and knowledge of each individual’s case prevented more crimes than other courts and prevented more days of drug use. And, when drug court participants reported more positive attitudes toward their judge, they cut drug use and crime even more.
While drug court costs are higher than business-as-usual case processing, they save money, the study determined, by significantly reducing the number of crimes, re-arrests, and days incarcerated. Drug courts save an average of $5,680 per participant, returning a net benefit of $2 for every $1 spent.

The Study

Drug courts emerged in the late 1980s and early 1990s as drug arrests and prosecutions exploded, overwhelming traditional courts’ capacity to process cases expeditiously.
The Multi-Site Adult Drug Court Evaluation, funded by the U.S. Department of Justice’s National Institute of Justice, was conducted in two phases. The first, in 2004, surveyed 380 drug courts, more than half of which required both an eligible charge and a clinical assessment for offenders to enrol. Few courts allowed participants with prior convictions for violent misdemeanour or felony offences. More than a third of courts served only those who were diagnosed as addicted to or dependent on drugs; others also served regular users or those with any level of use.
In the study’s second phase, researchers selected 23 drug courts in Florida, Georgia, Illinois, New York, Pennsylvania, South Carolina, and Washington, and six comparison sites in Florida, Illinois, North Carolina, and Washington. Between March 2005 and fall 2009, the team visited each location multiple times to document program characteristics and operations; interviewed a sample of 1,156 drug court participants and 625 comparison group members as many as three times (baseline interview and interviews 6 and 18 months later); administered a drug test at the 18-month mark; and obtained criminal histories, recidivism data, and budget information from state agencies and the FBI.

More Key Findings

Drug court participants who perceived the consequences of failing the program as more undesirable engaged in less substance use and crime. And those who received more judicial supervision and drug testing, or who attended more than 35 days of substance abuse treatment, reported fewer crimes and fewer days of drug use.
Drug court participants, compared to similar offenders processed through standard dockets, reported fewer days of drug use (2.1 vs. 4.8 days per month) and fewer crimes committed (52.5 vs. 110.1) when questioned about the past year at the 18-month interview.
Relative to similar offenders in the comparison group, those initially reporting more frequent drug use showed a larger reduction in drug use at the 18-month interview. Offenders with violent histories had a greater reduction in crime than others.
Although drug courts prevent a great deal of small-cost crime, overall savings are driven by a reduction in the most serious offending by relatively few individuals. Drug courts are especially likely to save money, therefore, if they enrol serious offenders.
The Takeaways: Implications for Policy and Practice
The researchers recommend that
judges hold frequent judicial status hearings, especially for high-risk participants;
administrators assign judges who are committed to the drug court model;
judges get training on best practices regarding judicial demeanour and effective communication with participants;
courts broaden participant eligibility, particularly to include those with mental health problems and histories of violent offences;
programs include sufficient drug treatment; and
courts administer drug tests more than once a week during the program’s initial phase

Source: http://www.urban.org/url.cfm?ID=901438 July 18th 2011

In this Dutch study, promoting parental rule setting and classroom alcohol education together nearly halved the proportion of adolescents who went on to drink heavily. Rarely have such strong and sustained drinking prevention impacts been recorded from these types of interventions.

Summary

This Dutch study tested the long-term impact of the Örebro intervention (first developed and tested in Sweden) targeting parental rule-setting in relation to the drinking of their adolescent children, allied with classroom alcohol education. The parenting element entailed a brief presentation from an alcohol expert at the first parents’ meeting at the start of each school year on the adverse effects of youth drinking and the negative effects of permissive parental attitudes towards children’s alcohol use. After this parents of children from the same class were meant to meet to agree a shared set of rules about alcohol use. In fact, only half the schools did this; the remainder used the later mailing to send a checklist of candidate rules to parents for them to select from and return to the school. Three weeks after this meeting, a summary of the presentation and the result of the classroom discussion was sent to parents’ home addresses. Classroom alcohol education consisted of four lessons from trained teachers at the schools plus a booster a year later, using mainly computerised modules to foster a healthy attitude to drinking and to train the pupils in how to refuse offers of alcohol.
The 19 schools which joined the study were randomly allocated to the parenting intervention alone, to classroom alcohol education alone, to the combination of both, or to act as control schools which carried on with alcohol education as usual.
An earlier paper from the same study reported that relative to education as usual, among the 2937 (of 3490) 12–13-year-olds not already drinking weekly and who met other criteria for the study, the combined parenting and education intervention curbed the initiation of weekly drinking and heavy weekly drinking over the next 22 months (and reduced the frequency of drinking). In contrast, on their own, neither the parenting elements nor the lessons made any significant difference when the whole sample of children not yet drinking weekly at the start were included in the analyses.

Main findings

The featured report tested whether these effects were still apparent a year later, 34 months after the start of the study and when the pupils averaged just over 15 years of age, a time when two thirds of Dutch youngsters are already drinking weekly and will soon (age 16) be able to legally buy alcohol. Of the 2937 in the initial sample of non-weekly drinkers, 2533 (86%) completed the follow-up assessment. The probable responses of the remainder were estimated on the basis of prior assessments and other data. As before, the parenting elements or alcohol education alone had made no statistically significant differences to drinking, but the impacts of both together in retarding uptake of weekly and heavy weekly drinking were greater than a year before chart. Compared to 59% and 27% in education-as-usual control schools, after the combined intervention 49% and 15% of pupils were drinking weekly or drinking heavily each week. After adjusting for other factors, the results meant that in combined intervention schools, the odds of these patterns of drinking versus less extreme drinking had been reduced to 0.69 relative to education as usual, highly statistically significant findings. Put another way, for every four pupils allocated to parenting plus alcohol education, one was prevented from drinking weekly and also one from drinking heavily each week at age 15.

The authors’ conclusions

In a liberal drinking culture where adolescent and underage drinking is common, targeting both parents and young adolescent pupils (but not either on their own) exercises a sustained and substantial restraining influence on the development of regular and regular heavy drinking as the youngsters approach the legal alcohol purchase age. The findings underline the need to target adolescents as well as their parents and of targeting adolescents at an early age, before they start to drink regularly and when family factors are a major influence on youth drinking. Doing so has the potential to create appreciable public health gains.

Source: Koning I.M., van den Eijnden R.J., Verdurmen J.E. et al.
American Journal of Preventive Medicine: 2011, 40(5), p. 541–547.

Smoking is an important risk factor in brain shrinkage and a decline in brain function in later years, a new study suggests. The study found smoking, along with high blood pressure, diabetes and excess weight, all contributed to potentially dangerous changes in the brain that could lead to a decline in mental functioning as soon as 10 years later. The study appears in the journal Neurology.
HealthDay reports the study included 1,352 people without dementia whose average age was 54. Each person was weighed, measured, given blood pressure, cholesterol and diabetes tests and underwent brain MRI scans over 10 years. The researchers found smokers lost brain volume overall and in the hippocampus—the part of the brain which converts short-term memory into long-term memory—at a faster rate than nonsmokers. They were also more likely to have a rapid increase in small areas of damage to the brain’s blood vessels.
Study author Charles DeCarli, M.D., of the University of California at Davis Alzheimer’s Disease Center, said in a journal news release, “Our findings provide evidence that identifying these risk factors early in people of middle age could be useful in screening people for at-risk dementia and encouraging people to make changes to their lifestyle before it’s too late.”

Source: ThePartnership @drugfree.org. Aug.2011

Men who use marijuana may increase their risk for developing testicular cancer. A
recent study of several hundred Washington State men with testicular cancer showed an association between current marijuana use and the more aggressive of the two types of the disease. Moreover, the association was strongest among men with a long history of regular marijuana use.

To firmly link marijuana use and the cancer, however, scientists will need to replicate the findings among large groups of men across many geographical regions and identify the underlying biological mechanisms, says NIDA-funded researcher Dr. S. K. Dey of the Cincinnati Children’s Hospital Medical Center, who collaborated on the study with Drs. Janet Daling and Stephen M. Schwartz and colleagues at the Fred Hutchinson Cancer Research Center and the University of Washington.

During the past 50 years, the number of new cases of testicular cancer reported annually in the United States has nearly doubled. So has the percentage of the general population who report having smoked marijuana at least once. Dr. Dey suspected that the two trends might be related, although exposure to various environmental factors may also be involved. Along with the simultaneous rise in rates, there are biological reasons to hypothesize a connection between the drug and the cancer. Research has shown that marijuana smoking reduces sperm production and male fertility, and other work has linked diminished fertility to increased risk of testicular cancer. Cannabinoid receptors— the cell-membrane proteins that bind to a component of marijuana as well as to the naturally occurring compounds known as endocannabinoids—occur on the cell
membranes of sperm, the testes (see photograph), the uterus, and embryos, as well as on brain neurons. Marijuana smoking causes widespread effects in the endocrine and reproductive systems and might alter the growth of somatic and germ cells in the testes, resulting in testicular cancer.

The research team interviewed 369 men who were diagnosed with testicular cancer between 1999 and 2006 and 979 men who never had the disease. They recruited all of the study participants from three counties in Washington State and controlled statistically for smoking, drinking, and other testicular cancer risk factors. Approximately 70 percent of each group reported smoking marijuana at least once. The researchers found that the odds of having testicular cancer were 70 percent higher among men who reported current marijuana use compared with nonusers. In addition, the researchers observed 80 percent higher odds of testicular cancer among men who started to use marijuana before age 18 compared with nonusers. They also found that the odds for testicular cancer among men who used marijuana at least weekly were twice that of nonusers.

Of the two categories of testicular cancer, nonseminomas and seminomas, the former was strongly associated with a history of marijuana smoking, but the latter had little or no association, Dr. Dey says. Nonseminomas occur in younger men, grow more rapidly, and have lower survival rates. While a man diagnosed with seminomas is 98 percent as likely as someone without the disease to still be alive 10 years later, the figure for someone diagnosed with a nonseminoma ranges from 46 percent to 92 percent, depending on the tumor subtype.
The association between marijuana smoking and nonseminomas, but not seminomas, is difficult to explain, says Dr. Dey. The rates for both types of cancer have been rising, and subnormal fertility and certain environmental exposures during puberty—such as chemicals that affect estrogen and androgen production—are risk factors for both.
“My colleagues and I hope our study sparks similar epidemiological investigations of the relationship between testicular cancer and marijuana abuse around the world,” says Dr. Dey. “These results may also spur animal research, which is essential for interpreting our findings.” Animal research, he says, will be required to determine whether marijuana’s psychoactive ingredient, delta-9 tetrahydrocannabinol (THC), or its other components increase the risk of testicular cancer. Studies with animals may also search for molecular pathways connecting marijuana and testicular cancer. Such studies would probably focus
on marijuana’s activation of the neurotransmitter system that underlies its psychoactive, endocrine, and reproductive effects.
“If these interesting findings are replicated in a large, nationally representative group of participants, then future research should delve into the molecular mechanism underlying the association,” says Dr. Vishnudutt Purohit of NIDA’s Division of Basic Neuroscience and Behavioral Research. He notes that the study by Drs. Dey, Daling, and Schwartz is part of NIDA-supported research to determine how drugs of abuse affect the cardiovascular, pulmonary, reproductive, and immune systems of the body.
(For more information on these cancers, see http://seer.cancer.gov/publications/survival/surv_testis.pdf.)

SOURCE
Daling, J.R., et al. Association of marijuana use and the incidence of testicular germ cell tumors. Cancer 115(6):1215–1223, 2009.
December 2010 NIDA Notes/ Volume 23, Number 3

Celebrities and millionaires with no history of addiction research or helping addicts to reclaim destroyed lives campaigned globally in June to make drugs even more available – citing reasons based on theory not fact. David Raynes tells the truth

COMPARE STATISTICS: HARMS OF LEGAL vs ILLEGAL DRUGS

• “More deaths are caused each year by tobacco use than by all deaths from HIV, illegal drug use, alcohol use, motor vehicle injuries, suicides, and murders combined,” states the US Centre for Disease Control (www.cdc.gov/tobacco/data_ statistics/fact_sheets/health_effects/tobacco_related_
mortality). UK figures are below.

• 880 deaths/year involve heroin or morphine
(latest figures from the Office of National Statistics at http://www.statistics.gov.uk/pdfdir/poi0311.pdf)

• 8,664 deaths/year involve alcohol (http://www.statistics.gov.uk/cci/nugget.asp?id=1091

• 81,400 deaths of people in England alone aged 35+ were attributable to tobacco (http://www.ic.nhs.uk/pubs/smoking10)

• An estimated 462,900 hospital admissions in England alone of people aged 35+ were attributable to smoking (ibid).

Source: Addiction Today July/August 2011

People who abused methamphetamine or other amphetamine-like stimulants were more likely to develop Parkinson’s disease than those who did not, in a new study from the Centre for Addiction and Mental Health (CAMH).
The researchers examined almost 300,000 hospital records from California covering 16 years. Patients admitted to hospital for methamphetamine or amphetamine-use disorders had a 76 per cent higher risk of developing Parkinson’s disease compared to those with no diagnosis. Globally, methamphetamine and similar stimulants are the second most commonly used class of illicit drugs.
“This study provides evidence of this association for the first time, even though it has been suspected for 30 years,” said lead researcher Dr. Russell Callaghan, a scientist with CAMH. Parkinson’s disease is caused by a deficiency in the brain’s ability to produce a chemical called dopamine. Because animal studies have shown that methamphetamine damages dopamine-producing areas in the brain, scientists have worried that the same might happen in humans.
It has been a challenge to establish this link, because Parkinson’s disease develops in middle and old age, and it is necessary to track a large number of people with methamphetamine addiction over a long time span. The CAMH team took an innovative approach by examining hospital records from California – a state in which methamphetamine use is prevalent – from 1990 up to 2005. In total, 40,472 people, at least 30 years of age, had been hospitalized due to a methamphetamine- or amphetamine-use disorder during this period.
These patients were compared to two groups: 207,831 people admitted for appendicitis with no diagnosis of any type of addiction, and 35,335 diagnosed with cocaine use disorders. A diagnosis of Parkinson’s disease was identified from hospital records or death certificates. Only the methamphetamine group had an increased risk of developing Parkinson’s disease.
While the appendicitis group served as a comparison to the general population, the cocaine group was selected for two reasons. Because cocaine is another type of stimulant that affects dopamine, this group could be used to determine whether the risk was specific to methamphetamine stimulants. Cocaine users also served as a control group to account for the health effects or lifestyle factors associated with dependence on an illicit drug.
“It is important for the public to know that our findings do not apply to patients who take amphetamines for medical purposes, such as attention deficit hyperactivity disorder (ADHD), since these patients use much lower doses of amphetamines than those taken by patients in our study,” said Dr. Stephen Kish, a CAMH scientist and co-author.
To put the study findings into numbers, if 10,000 people with methamphetamine dependence were followed over 10 years, 21 would develop Parkinson’s, compared with 12 people out of 10,000 from the general population. “It is also possible that our findings may underestimate the risk because in California, methamphetamine users may have had less access to health-care insurance and consequently to medical care,” said Dr. Callaghan.
The current project is significant because it is one of the few studies examining the long-term association between methamphetamine use and the development of a major brain disorder. “Given that methamphetamine and other amphetamine stimulants are the second most widely used illicit drugs in the world, the current study will help us anticipate the full long-term medical consequences of such problematic drug use,” said Dr. Callaghan.
Media Contact: Michael Torres, Media Relations, CAMH; 416-595-6015

Source: www.camh.net 26th July 2011

A new study by a team of researchers in California shows it is possible to vaccinate laboratory animals against the effects of heroin. The vaccine not only blunted the painkilling action of heroin, it also prevented rats from becoming addicted to the drug. It didn’t keep the animals from gaining pain relief from many other opiates, suggesting the vaccine targets just heroin and a few related compounds. The experiments at the Scripps Research Institute in La Jolla, reported in the current edition of the Journal of Medicinal Chemistry, are the latest effort to bring the power of the immune system to bear against addictive substances. The next task is to see whether the vaccine prevents relapse in previously addicted and then detoxified rats.

Source: Reported in St.Petersburg Times July 28th 2011

The story that broke one afternoon in mid-March was startling, even to editors who have been around for a while.
A 19-year-old man had died and 10 others were sickened in a mass overdose after experimenting with a synthetic drug during a party in Blaine.
We have written before about the problems of designer synthetic drugs, which are molecularly different from illegal drugs and sometimes can be acquired legally in shops or over the Internet. But this was the first time we had seen such deadly ramifications. After covering the case in Blaine, which resulted in one man being charged with third-degree murder, we set out to discover just how big a problem these drugs are posing in society. Our preliminary research revealed that this was a growing problem nationally, with devastating consequences across the country.
In the months since, we have researched or acquired dozens of these synthetic drugs, to discover how easy they are to buy and whether consumers are given any warnings at all when they buy the drugs.
We have talked to users, victims and witnesses across the country about some of the unintended consequences of ingesting synthetic drugs. And we have enlisted a number of experts, researchers and businesses in the greater Twin Cities community to help us identify what exactly is in the most common compounds so we can pinpoint the true risk to consumers. For example, Internet Exposure, a web development and marketing firm, is conducting research for us on how people are using the Internet to research and buy drugs, while MedTox Laboratories in St. Paul is testing chemicals for us.
The results of our investigation will unfold in stories that we will publish over the next few months, with the first appearing online today. It is a tragic story of a party that went wrong in a small town in Oklahoma, with eerie similarities to the party in Blaine earlier this year. We went to Oklahoma to illustrate that if synthetic drugs are a problem in such a small, tight-knit community like Konawa, they can create trouble anywhere in Middle America.
Police officer Kat Green, who arrives at the party in Oklahoma to find her own son nearly incapacitated, repeatedly wonders why her son would put something in his body without knowing exactly what it was.
Why indeed, would anyone?
The answer to that question seems to be that these partygoers are taking synthetic drugs because they think it will be fun, the drugs are often touted as legal, and the drugs are easily acquired, making them seem less dangerous than illegal drugs like marijuana, cocaine or hallucinogens. (Some people also take synthetic drugs because they may not show up on drug tests. )
Pamela Louwagie, who has been one of the primary reporters on this investigation, said that some of the partygoers in both Blaine and Oklahoma had researched the drugs they thought they were acquiring, while others “simply seemed to trust that their friends had done enough research to be safe.
“It was striking that, in each case, they didn’t get what was ordered,” Louwagie said. “That showcases the true danger in these things. Many of these substances, while they have been around … for a while, are truly untested. And if you buy them, you don’t know what they have been mixed with and, in some cases, whether you’re even getting the right thing.”
What’s also striking is the trust buyers put in the notion that it is safe to acquire a synthetic drug over the Internet, from an unproven source.
We hope that when we have finished our investigation, we will have helped parents, teenagers and other adults truly understand the risk that synthetic drugs pose — as well as the dangers of buying substances from some unknown source somewhere around the globe who just happens to advertise on the Internet.
I’ll be sharing this story with my own daughters; I urge others to share it with friends and family as well.

Source: Nancy Barnes, Editor, www. StarTribune.com 24th July 2011

A new study suggests that abuse of prescription opioids may be a first step on the path toward misuse of heroin and other injected drugs.
Science Daily reports that the researchers found four out of five injection drug users misused an opioid drug before they injected heroin. They also found that almost one out of four young injection drug users first injected a prescription opioid, and most later switched to injecting heroin.
The study, published in the International Journal of Drug Policy, found that risk factors for misusing opioid drugs include family history of drug misuse, and a past history of receiving prescriptions for opioids.
“Participants were commonly raised in households where misuse of prescription drugs, illegal drugs, or alcohol, was normalized,” lead researcher Dr. Stephen Lankenau, from Drexel University in Philadelphia, said in a news release. “Access to prescription medications – either from a participant’s own source, a family member, or a friend – was a key feature of initiation into prescription drug misuse.”
The study included 50 injection drug users between the ages of 16 to 25. They had all misused a prescription drug at least three times in the past three months. Nearly three-fourths of participants had been prescribed an opioid, often for dental procedures or sports injuries. Most had family members who misused one or more substances. The authors called on parents to carefully monitor and safeguard prescription drugs, especially opioids, in their home

Source: International Journal of Drug Policy June 2011

Electronic cigarettes, or “e-cigarettes,” are crude drug delivery systems for refined nicotine that pose unknown risks, two experts write in this week’s New England Journal of Medicine. Researchers from the American Legacy Foundation’s Steven A. Schroeder National Institute for Tobacco Research and Policy Studies write that e-cigarettes have more in common with asthma inhalers than with cigarettes, according to Science Daily.
E-cigarettes are designed to deliver nicotine in the form of a vapor, which is inhaled by the user. They usually have a rechargeable, battery-operated heating element, a replaceable cartridge with nicotine or other chemicals and a device called an atomizer that converts the contents of the cartridge into a vapor when heated. E-cigarettes often are made to look like regular cigarettes.
The Food and Drug Administration (FDA) announced in April that it would regulate e-cigarettes as tobacco products, not as drug-delivery devices.
Last year, the FDA lost a court case after it tried to treat e-cigarettes as drug-delivery devices, which must satisfy stricter requirements than tobacco products, including clinical trials to prove they are safe and effective. FDA tests found that the liquid in some e-cigarettes contained toxins besides nicotine, as well as cancer-causing substances found in tobacco. Some public health experts say the level of the cancer-causing agents is similar to those found in nicotine replacement therapy, which contains nicotine extracted from tobacco.
The authors list several safety concerns about e-cigarettes. They note that the devices do not reliably deliver nicotine, and have not been sufficiently studied in the same way the FDA requires other smoking-cessation drugs and devices to be evaluated. Therefore, smokers who try to use e-cigarettes to help them quit smoking are likely to find them ineffective because of their variable nicotine content and unreliable delivery, they say.
They also note that smokers may use e-cigarettes in places where traditional tobacco smoking is not allowed, thus encouraging them to keep smoking instead of quitting. E-cigarettes also may become a smoking “starter” product for young people. E-cigarette cartridges can be bought over the Internet with flavors such as chocolate and grape, they write.

Source: DrugFreee.org 21st July 2011

Women who smoke while pregnant should be aware that they are increasing the chance their baby will be born malformed, say experts.
The risk for having a baby with missing or deformed limbs or a cleft lip is over 25% higher for smokers, data show. Along with higher risks of miscarriage and low birth weight, it is another good reason to encourage women to quit, say University College London doctors.
In England and Wales 17% of women smoke during pregnancy. And among under 20s the figure is 45%. Although most will go on to have a healthy baby, smoking can cause considerable damage to the unborn child.
Missing limbs
Researchers now estimate that each year in England and Wales several hundred babies are born with a physical defect directly caused by their mother’s smoking. Every year in England and Wales around 3,700 babies in total are born with such a condition. The experts base their calculations on 172 research papers published over the last 50 years, which looked at maternal smoking and birth defects.
The findings, from 174,000 cases of malformation and 11.7 million healthy births, revealed that smoking increased the risk of many abnormalities. The chance of a baby being born with missing or deformed limbs is 26% higher, and cleft lip or palate is 28% more likely.
Similarly, the risk of clubfoot 28% greater, and gastrointestinal defects 27% more. Skull defects are 33% more likely, and eye defects 25% more common. The greatest increase in risk – of 50% – was for a condition called gastroschisis, where parts of the stomach or intestines protrude through the skin. Professor Allan Hackshaw, who led the research, suspects many women who smoke while pregnant do not know about these risks.
“There’s still this idea among some women that if you smoke the baby will be small and that will make it easier when it comes to the delivery. “But what is not appreciated is that smoking during pregnancy increases the risk of defects in the child that are life-long.”
Women should quit smoking before becoming pregnant, or very early on, to reduce the risks
He said very few public health educational policies mention birth defects when referring to smoking and those that do are not very specific – this is largely because of past uncertainty over which ones are directly linked. “Now we have this evidence, advice should be more explicit about the kinds of serious defects such as deformed limbs, and facial and gastrointestinal malformations that babies of mothers who smoke during pregnancy could suffer from,” he said.
Of the 700,000 babies born each year in England and Wales, around 120,000 babies are born to mums who smoke. Amanda Sandford of Action on Smoking and Health said: “This study shows some of the worst outcomes of smoking during pregnancy. Pregnant smokers will be shocked to learn that their nicotine habit could cause eye or limb deformities in their baby.
“There is clearly a need to raise awareness of these risks among girls and to ensure pregnant women are given all the support they need to help them quit smoking and to stay stopped after the birth.” Basky Thilaganathan of the Royal College of Obstetricians and Gynaecologists said women who struggled to quit should at least cut down on how much they smoke.
Professor Hackshaw said the risk was likely dose-related – meaning the more a woman smokes, the bigger the risk to her unborn child.

Source: www.bbc.co.uk 12th July 2011

Researchers from the Medical Research Council (MRC) have uncovered for the first time how excess alcohol can cause irreparable damage to our DNA. In a new study published in the journal Nature today, MRC scientists also discovered a two-tier defence system in our cells that limits the threat of permanent genetic damage.
Scientists at the MRC’s Laboratory of Molecular Biology (LMB) have discovered that an overload of a toxic chemical called acetaldehyde, a by-product from the breakdown of alcohol in our body, can cause damage to DNA. They showed that our cells have two natural ways of protecting us against acetaldehyde. Firstly, this toxin can be removed by specialised enzymes. If this step fails, acetaldehyde builds up and damages DNA, but a second mechanism kicks in to repair the damaged DNA, using another set of enzymes known as the Fanconi proteins.
In pregnant mice which were genetically altered not to have these two defences, the equivalent of a single binge drinking session of alcohol caused catastrophic damage to the fetus. Not only did alcohol damage the fetus, but in the adult modified mice, this alcohol consumption damaged blood stem cells, obliterating the production of blood.
Dr KJ Patel, lead author of the paper from the MRC Laboratory of Molecular Biology, said:
“The findings show how critically reliant we are on both these control systems to prevent alcohol from causing irreversible mutations to DNA, both in the fetus and in our own cells.
“The effects of alcohol in the modified pregnant mice resembled fetal alcohol syndrome, where excessive drinking by pregnant women causes permanent damage to the unborn child, leading to birth defects and learning difficulties. Our work suggests that binge drinking could generate enough acetaldehyde to overwhelm the body’s two natural defence mechanisms.
“This new knowledge transforms our view of precisely how excess alcohol causes damage – ultimately changing our DNA. Quite apart from this, our conclusions suggest potentially simple approaches to treat Fanconi anaemia – currently a terminal incurable illness in humans.”
The study highlights how two groups who have inherited failures of the natural control mechanisms are particularly at risk of severe DNA damage from alcohol. Individuals with a rare disease called Fanconi anaemia, which affects around 20,000 people worldwide, do not have the enzymes which repair DNA and are likely to be very sensitive to acetaldehyde. This could explain why such people are highly susceptible to both blood disorders and cancer. More commonly, around 500 million people from South East Asia with a condition called the ‘Asian alcohol flushing mutation’ have a greatly reduced capacity to break down acetaldehyde. This research suggests these individuals may be susceptible to lifelong DNA damage and could explain why alcohol consumption greatly increases their risk of gullet cancer.
Dr Hugh Pelham, director of the MRC Laboratory of Molecular Biology, said:
“We know that there’s a complex interplay between genetics, our body’s natural resilience to disease and our environment. By determining the molecular reason behind the toxic effects of alcohol to our DNA, our researchers have shown how vulnerable we can be to DNA damage from excess alcohol and even more so in the womb. Despite the existence of protective mechanisms, long-term genetic damage must be added to the risks of excessive alcohol consumption.”
The research was also funded by the Children’s Leukaemia Trust UK and the Fanconi Anaemia Research Fund USA.

Source: www.mrc.ac.uk 6th July 2011

Finding could lead to development of drugs that decrease heavy alcohol consumption.

A team of Scripps Research Institute scientists has found a key biological mechanism underpinning the transition to alcohol dependence. This finding opens the door to the development of drugs to manage excessive alcohol consumption.
“Our focus in this study, like much of our lab’s research, was to examine the role of the brain’s stress system in compulsive alcohol drinking driven by the aversive aspects of alcohol withdrawal,” said Scripps Research Associate Professor Marisa Roberto, Ph.D., senior author of the study.
“A major goal for this study,” added Research Associate Nicholas Gilpin, Ph.D., the paper’s first author, “was to determine the neural circuitry that mediates the transition to alcohol dependence.”
In the new research, published in the June 1, 2011 issue of the journal Biological Psychiatry, the Scripps Research scientists demonstrated the key role of a receptor —a structure that binds substances, triggering certain biological effects—for neuropeptide Y in a part of the brain known as the central amygdala. The amygdala, a group of nuclei deep within the medial temporal lobes, performs an important role in the processing and memory of emotional reactions.
“We’ve known for quite some time that neuropeptide Y is an endogenous [naturally occurring] anti-stress agent,” says Markus Heilig, clinical director of the National Institute of Alcohol Abuse and Alcoholism (NIAAA). “We’ve also known that development of alcohol dependence gives rise to increased sensitivity to stress. This paper elegantly and logically brings these two lines of research together. It supports the idea that strengthening neuropeptide Y transmission in the amygdala would be an attractive treatment for alcoholism. The challenge remains to develop clinically useful medications based on this principle.”
Discovering the Circuitry
Building on Gilpin’s previous work on neuropeptide Y, in the new project, Gilpin, Roberto, and colleagues observed the effects of the administration neuropeptide Y in the central amygdala on alcohol drinking in rats. Alcohol-dependent rats were allowed to press levers for ethanol and water during daily withdrawal from chronic alcohol exposure.
“Normally, the transition to alcohol dependence is accompanied by gradually escalating levels of alcohol consumption during daily withdrawals,” Gilpin explained. “The aim of this protocol was to examine whether neuropeptide Y infusions during daily withdrawals would block this escalation of alcohol drinking.”
The scientists report a suppression of alcohol consumption with chronic neuropeptide Y infusions and detailed some of the neurocircuitry involved. Ethanol normally produces robust increases in inhibitory GABAergic transmission—GABA is another neurotransmitter—in the central amygdala, but this effect is blocked and reversed by neuropeptide Y.
Gilpin notes the scientists were surprised at one aspect of the findings—the role of a subset of neuropeptide Y receptors known as Y2 receptors. “Previous behavioral evidence suggested that antagonism of Y2 receptors in whole brain suppresses alcohol drinking, similar to the effects of neuropeptide Y,” he said. “However, our data suggest that Y2 receptor blockade in central amygdala might actually increase alcohol drinking, presumably by affecting pre-synaptic release of GABA. These data also suggest that antagonism of post-synaptic Y1 receptors in central amygdala provides a viable pharmacotherapeutic strategy, a hypothesis supported by previous work from other labs.”
Two additional aspects of the findings are worth noting, Roberto says. First, repeated neuropeptide Y administration not only blocked the development of excessive alcohol consumption in dependent rats, but also tempered the moderate increase in alcohol consumption following periods of abstinence in non-dependent rats. Second, neuropeptide Y exhibited long-term efficacy in suppressing alcohol self-administration, highlighting the potential of neuropeptide Y treatments for a clinical setting.

Source: “Neuropeptide Y Opposes Alcohol Effects on GABA Release in Amygdala and Blocks the Transition to Alcohol Dependence” June 1, 2011 print edition of Biological Psychiatry. See http://www.ncbi.nlm.nih.gov/pubmed/21459365