2011 March

For health care workers in psychiatric hospitals, it is no secret: one of the major issues confronting psychiatric facilities seeking to institute blanket no-smoking policies concerns chronic inpatients with schizophrenia. Patients with schizophrenia are almost always heavy cigarette smokers, given a choice. As Edward Lyon wrote in an analysis of studies and surveys performed throughout the 1990s: “Many patients in psychiatric hospitals would smoke two, three, or even four packs of cigarettes a day if an unlimited supply of cigarettes were available.”
Generally, the rate of inpatient smoking among schizophrenics is three to four times higher than the general smoking population. In one British study of 100 institutionalized schizophrenics cited by Lyon, 92% of the men and 82% of the women were smokers. Moreover, schizophrenics smoke more cigarettes per day than other smokers do, and they commonly smoke high-tar, unfiltered cigarettes — niche brands for heavy smokers used by only 1% of the total smoking population.
Australian research performed in 2001 found that because of high rates of smoking, “people with mental illness have 30% more heart disease and 30% more respiratory disorders,” according to Ann Crocker, now a professor of Clinical Psychiatry at McGill University.
Not only do an estimated 80% of schizophrenics smoke, compared to roughly 25% of the total adult population, psychiatric facilities report that depressives and those with anxiety disorders also smoke in great numbers.
Why?
The review of studies through 1999, undertaken by Lyon and published in Psychiatric Services, shows unequivocally that schizophrenic smokers are self-medicating to improve processing of auditory stimuli and to reduce many of the cognitive symptoms of the disease. “Neurobiological factors provide the strongest explanation for the link between smoking and schizophrenia,” Lyons writes, “because a direct neurochemical interaction can be demonstrated.”
Of particular interest is the interaction between nicotine and dopamine in the nucleus accumbens and prefrontal cortex. Several of the symptoms of schizophrenia appear to be associated with dopamine release in these brain areas. A 2005 German study concluded that nicotine improved cognitive functions related to attention and memory. “There is substantial evidence that nicotine could be used by patients with schizophrenia as a ‘self-medication’ to improve deficits in attention, cognition, and information processing and to reduce side effects of antipsychotic medication,” the German researchers concluded.
In addition, the process known as “sensory gating,” which lowers response levels to repeated auditory stimuli, so that a schizophrenic’s response to a second stimulus is greater than a normal person’s, is also impacted by cigarettes. Sensory gating may be involved in the auditory hallucinations common to schizophrenics. Receptors for nicotine are involved in sensory gating, and several studies have shown that sensory gating among schizophrenics is markedly improved after smoking.
There is an additional reason why smoking is an issue of importance for health professionals. According to Lyon, “Several studies have reported that smokers require higher levels of antipsychotics than nonsmokers. Smoking can lower the blood levels of some antipsychotics by as much as 50%…. For example, Ziedonis and associates found that the average antipsychotic dosage for smokers in their sample was 590 mg in chlorpromazine equivalents compared with 375 mg for nonsmokers.”
Smoking among inpatient psychiatric patients is not trivial. Neither is the decision to institute smoking bans in psychiatric hospitals, a move that is understandably unpopular with patients.
References
Lyon, E. (1999). A Review of the Effects of Nicotine on Schizophrenia and Antipsychotic Medications. Psychiatric Services, 50, 1346-1350.
Cattapan-Ludewig, K. (2005). Why do schizophrenic patients smoke? Nervenarzt, 76 (3), 287-294.
Mueser, K., Crocker, A., Frisman, L., Drake, R., Covell, N., & Essock, S. (2005). Conduct Disorder and Antisocial Personality Disorder in Persons With Severe Psychiatric and Substance Use Disorders Schizophrenia Bulletin, 32 (4), 626-636 DOI: 10.1093/schbul/sbj068
Adler, L., Hoffer, L. Wiser, A. (1993). Normalization of auditory physiology by cigarette smoking in schizophrenic patients. American Journal of Psychiatry, 150, 1856-1861.

Source: http://brainblogger.com/2009/07/03/why-do-schizophrenics-smoke-cigarettes/
3rd July 2009

Filed under: Social Affairs (Papers) :

Are young smokers risking cognitive impairment as adults? Call it “nicolescence.” It’s that time of life when certain 18-and-unders discover cigarettes. Most adult smokers begin their habit before the age of 19, and a majority of adolescents have tried cigarettes at least once. But for some of them—those who were “born to smoke,” in a sense—early exposure to nicotine may influence adolescent cognitive performance in ways that adult exposure to nicotine does not. Furthermore, early exposure may result in “cognitive impairments in later life.”

These provocative notions are raised by a group of researchers at VU University, Amsterdam, The Netherlands, in a paper for Nature Neuroscience. And while the specifics of glutamate activity they have documented are fascinating, the leaps back and forth between adolescent humans and adolescent lab mice are dizzying. Nonetheless, the bold claims made in the paper prompted the scientists “to reconsider our views on the etiology of attention deficits.”

That may be more than many addiction researchers are willing to countenance, but the study makes an intriguing case for long-term effects on attentional processing. The Dutch researchers exposed adolescent rats to nicotine, assessed visuospatial attention and other markers associated with synaptic activity in the prefrontal cortex, and found impaired measures of attention and signs of increased impulsivity in adulthood after five weeks of abstinence. Adult rats exposed to nicotine for the first time did not show similar long-term consequences.

The molecular underpinnings for this phenomenon appear to be reduced glutamate receptor protein levels in the prefrontal cortex. Glutamate is a neurotransmitter involved in attention, among other cortical tasks. Glutamate levels were “altered specifically by adolescent and not adult nicotine exposure” in the lab animals, the researchers found.

The glutamate receptor mGluR2 is the likely culprit. The researchers report that “a lasting downregulation of mGluR2 on presynaptic terminals of glutamatergic synapses in the prefrontal cortex persists into adulthood causing disturbances in attention…. Restoring mGluR2 activity in vivo in the prefrontal cortex of adult rats exposed to nicotine during adolescence remediated the attention deficit.”

The study concludes: “Not only from a behavioral, but also from a molecular point of view, the adolescent brain is more susceptible to consequences of nicotinic receptor activation.” In other words, there is at least some evidence that the neurotoxic effects of nicotine are potentially more severe in the early developmental stage called adolescence.

The Dutch study is not the only one of its kind. In 2005, Biological Psychiatry published a report on cognition in which adolescent smokers “were found to have impairments in accuracy of working memory performance irrespective of recency of smoking. Performance decrements were more severe with earlier age of onset of smoking.”

And a 2007 study published in Neuropsychopharmocology, based on testing and fMRI scans of 181 male and female adolescent smokers, concluded that “in humans, prenatal and adolescent exposure to nicotine exerts gender-specific deleterious effects on auditory and visual attention…” Boys were more sensitive than girls to attention deficits involving auditory processing, while girls tended to show equal deficits in both auditory and visual attention tasks.

Counotte, D., Goriounova, N., Li, K., Loos, M., van der Schors, R., Schetters, D., Schoffelmeer, A., Smit, A., Mansvelder, H., Pattij, T., & Spijker, S. (2011). Lasting synaptic changes underlie attention deficits caused by nicotine exposure during adolescence Nature Neuroscience DOI: 10.1038/nn.2770

Source: http://addiction-dirkh.blogspot.com/2011/02/smoking-and-adolescent-attention.html 24th Feb 2011

COLUMBUS, Ohio – The federal anti-drug campaign “Above the Influence” appears to have effectively reduced marijuana use by teenagers, new research shows. A study of more than 3,000 students in 20 communities nationwide found that by the end of 8th grade, 12 percent of those who had not reported having seen the campaign took up marijuana use compared to only 8 percent among students who had reported familiarity with the campaign.

Evidence for the success of “Above the Influence” is especially heartening because the primary independent evaluation of its predecessor campaign, “My Anti-Drug”, showed no evidence for success, said Michael Slater, principal investigator of the new study and professor of communication at Ohio State University. “The ‘Above the Influence’ campaign appears to be successful because it taps into the desire by teenagers to be independent and self-sufficient,” Slater said. For example, one television ad in the campaign ends with the line “Getting messed up is just another way of leaving yourself behind.”
Campaigns that only emphasize the risk of drug use may not be effective with many teens.
“We know that many teenagers are not risk avoidant, and consider the risks of marijuana to be modest. A campaign that merely emphasizes already-familiar risks of marijuana probably won’t reach the teens who are most likely to experiment with drugs,” he said.
The study appears in the March 2011 issue of the journal Prevention Science.
Slater said this study was not originally designed to study the effectiveness of the “Above the Influence” campaign, which is sponsored by the federal Office of National Drug Control Policy (ONDCP). Instead, the study was going to examine the effectiveness of a very similar, but more localized anti-drug campaign called “Be Under Your Own Influence.” This theme was developed years before the “Above the Influence” campaign by study co-author Kathleen Kelly, professor of marketing at Colorado State University.
It involved in-school media and promotional materials combined with community-based efforts. Like the “Above the Influence” campaign, it emphasized that drug use undermines the ability of teens to achieve their goals and act independently. Slater said that members of his research team presented preliminary results supporting the effectiveness of “Be Under Your Own Influence” to the ONDCP and to Partnership for Drug Free America, which oversees creative efforts for the national campaign, in 2003, about two years before “Above the Influence” was launched. However, the researchers did not have any direct input into the development of the “Above the Influence” campaign.
Slater said the approaches are very similar. ‘Above the Influence’ uses the same approach — focusing on the inconsistency of substance use with teens’ aspirations and autonomy — that we developed,” he said.
A study published in 2006 of “Be Under Your Own Influence” showed that it reduced by about half the number of students who began using marijuana and alcohol during the two years of the project, compared to students in communities without the program. This new study was designed to replicate and extend the previous research, Slater said. In the 20 communities involved in the study, schools received some combination of some, all or none of the “Be Under Your Own Influence” materials.
The researchers surveyed 3,236 students who were about 12 years old when the study began in 2005. They were surveyed four times beginning in 7th grade and ending about a year and a half later. The researchers didn’t know that the ONDCP would be launching its “Above the Influence” campaign about the same time this new study began. As a result, though, the researchers asked students about their exposure to the national campaign during the second through fourth surveys.
The results of this study showed that the ONDCP campaign appeared to be very successful at reaching students: up to 79 percent of students surveyed said they had seen the ads. “There was wide exposure to the national campaign, and it really swamped the effects of our local effort,” Slater said. “It took over, and we didn’t see any independent effects for the ‘Be Under Your Own Influence’ campaign.”
But it was really the message of “Above the Influence” that mattered in reducing marijuana use – not the fact that it was a national campaign, he said. In their previous study, the researchers found that “Be Under Your Own Influence” showed strong local anti-drug effects, even though the national “My Anti-Drug” campaign was going on. “‘Above the Influence’ has succeeded more than its predecessor attempt to influence teens,” Slater said.
The effectiveness of the ONDCP campaign can be seen in the way it appeared to influence attitudes of teens who viewed the ads. Results showed that teens who had seen the “Above the Influence” ads were more likely than others to say that marijuana use was inconsistent with being autonomous and independent and that it would interfere with their goals and aspirations. “The teens seemed to pick up on the messages that the campaign promoted,” Slater said. “The campaign really works to honor teens’ interest in becoming autonomous and achieving goals and stays away from messages that don’t really reach the teens who are most likely to use marijuana.”
Slater says study limitations include the fact that findings regarding the ONDCP campaign were based on survey results and not a randomized, experimental design in which some youth saw the ONDCP campaign and others did not. Another limitation was that the study, while taking place in 20 communities around the U.S., did not use a random sample of U.S. youth.
Other co-authors of the study were Frank Lawrence of Penn State University; Linda Stanley of Colorado State University; and Maria Leonora G. Comello of the University of North Carolina.
The research was supported by a grant from the National Institute on Drug Abuse.

Source: http://researchnews.osu.edu/archive/aboveinfluence.htm March 2011

Filed under: Prevention (Papers) :

Risk appears to be elevated particularly among frequent and/or long-term users.

SEATTLE — February 9 — Frequent and/or long-term marijuana use may significantly increase a man’s risk of developing the most aggressive type of testicular cancer, according to a study by researchers at Fred Hutchinson Cancer Research Center. The study results were published online Feb. 9 in the journal Cancer.
The researchers found that being a marijuana smoker at the time of diagnosis was associated with a 70 percent increased risk of testicular cancer. The risk was particularly elevated (about twice that of those who never smoked marijuana) for those who used marijuana at least weekly and/or who had long-term exposure to the substance beginning in adolescence. The results also suggested that the association with marijuana use might be limited to nonseminoma, a fast-growing testicular malignancy that tends to strike early, between ages 20 and 35, and accounts for about 40 percent of all testicular-cancer cases.
Since the 1950s, the incidence of the two main cellular subtypes of testicular cancer, nonseminoma and seminoma – the more common, slower growing kind that strikes men in their 30s and 40s – has increased by 3 percent to 6 percent per year in the U.S., Canada, Europe, Australia and New Zealand. During the same time period, marijuana use in North America, Europe and Australia has risen accordingly, which is one of several factors that led the researchers to hypothesize a potential association.
“Our study is not the first to suggest that some aspect of a man’s lifestyle or environment is a risk factor for testicular cancer, but it is the first that has looked at marijuana use,” said author Stephen M. Schwartz, M.P.H., Ph.D., an epidemiologist and member of the Public Health Sciences Division at the Hutchinson Center. Established risk factors for testicular cancer include a family history of the disease, undescended testes and abnormal testicular development. The disease is thought to begin in the womb, when some fetal germ cells (those that eventually make sperm in adulthood) fail to develop properly and become vulnerable to malignancy. Later, during adolescence and adulthood, it is thought that exposure to male sex hormones coaxes these cells to become cancerous.
“Just as the changing hormonal environment of adolescence and adulthood can trigger undifferentiated fetal germ cells to become cancerous, it has been suggested that puberty is a ‘window of opportunity’ during which lifestyle or environmental factors also can increase the risk of testicular cancer,” said senior author Janet R. Daling, Ph.D., an epidemiologist who is also a member of the Center’s Public Health Sciences Division. “This is consistent with the study’s findings that the elevated risk of nonseminoma-type testicular cancer in particular was associated with marijuana use prior to age 18.”
Chronic marijuana exposure has multiple adverse effects on the endocrine and reproductive systems, primarily decreased sperm quality. Other possible effects include decreased testosterone and male impotency. Because male infertility and poor semen quality also have been linked to an increased risk of testicular cancer, this further reinforced the researchers’ hypothesis that marijuana use may be a risk factor for the disease.
Daling first got the idea to explore a possible association between marijuana use and testicular cancer about eight years ago, when she attended a talk by a physician at the University of Washington who presented findings that only two organs, the brain and the testes, had receptors for tetrahydrocannabinol, or THC, the main psychoactive component of marijuana. Since then, a number of other sites have been found to contain THC receptors, including the heart, uterus, spleen and immune-system cells. The male reproductive system also naturally produces a cannabinoid-like chemical that is thought to have a protective effect against cancer. The authors speculate that marijuana use may disrupt this anti-tumor effect, which could be another explanation for the possible link between marijuana and increased risk of testicular cancer.
For the population-based, case-control study, Daling, Schwartz and colleagues interviewed 369 Seattle-Puget Sound-area men, ages 18 to 44, who had been diagnosed with testicular cancer about their history of marijuana use. For comparison purposes they also assessed marijuana use among 979 randomly selected age- and geography-matched healthy controls. (More than 90 percent of the cases and 80 percent of the controls in the study were Hispanic or non-Hispanic white men, due to the fact that testicular cancer is very rare in African-Americans, and because the Seattle-Puget Sound region has a relatively small African-American population.)
Study participants were also asked about other habits that may be correlated with marijuana use, including smoking and alcohol consumption. Even after statistically controlling for these lifestyle factors, as well as other risk factors, such as first-degree family history of testicular cancer and a history of undescended testes, marijuana use emerged as a significant, independent risk factor for testicular cancer. The researchers emphasize that their results are not definitive, but rather open a door to more research questions.
“Our study is the first inkling that marijuana use may be associated with testicular cancer, and we still have a lot of unanswered questions,” Schwartz said, such as why marijuana appears to be associated with only one type of testicular cancer. “We need to conduct additional research to see whether the association can be observed in other populations, and whether measurement of molecular markers connected to the pathways through which marijuana could influence testicular cancer development helps clarify any association that exists,” he said.
In future studies the researchers plan to measure the expression of cannabinoid receptors in both seminomatous and nonseminomatous tumor tissue from the cases in the study, and to see whether variation in the genes for the receptors and other molecules involved in cannabinoid signaling influences the risk of testicular cancer. In the meantime, Schwartz said, “What young men should know is that first, we know very little about the long-term health consequences of marijuana smoking, especially heavy marijuana smoking; and second, our study provides some evidence that testicular cancer could be one adverse consequence,” he said. “So, in the absence of more certain information, a decision to smoke marijuana recreationally means that one is taking a chance on one’s future health.”
The National Cancer Institute, the National Institute on Drug Abuse and funds from the Hutchinson Center supported this research, which also involved researchers from the University of Washington, Vanderbilt University and Cincinnati Children’s Research Foundation. According to the National Cancer Institute, testicular cancer is very rare, accounting for only 1 percent of cancers in U.S. men. About 8,000 men are diagnosed with testicular cancer each year, and about 390 die of the disease annually. It is the most common form of cancer in men between the ages of 15 and 34 and is most common in white men, especially those of Scandinavian descent.

Source: journal Cancer. online Feb. 9 2011 Association of Marijuana Use and the Incidence of Testicular Germ Cell Tumors,”

Fred Hutchinson Cancer Research Center
1100 Fairview Ave. N. PO Box 19024 Seattle, WA 98109

Caria M.P., Faggiano F., Bellocco R. et al.
Journal of Adolescent Health: 2011, 48, p. 182–188.

The largest European drug education trial ever conducted tested whether US-style social influence programmes would prove effective in Europe. Among the successes were the reductions in problem drinking documented in this report.
Summary This account is partly based on an earlier Findings analysis of the same study.
Funded at European level by the European Commission, the European Drug Addiction Prevention trial (EU-Dap) aimed to test whether ‘social influence’ school-based drug prevention programmes of the kind developed in the USA will prove effective in Europe. Across seven countries and 170 schools it recruited 7079 12–14-year-old pupils, the largest sample ever in a European drug education trial.
Developed by the EU-Dap project team, the 12-lesson curriculum they tested is known in English as Unplugged. Materials are available on the EU-Dap web site and the programme’s development and approach has been extensively documented. As well as informing pupils about substances and their use, such curricula aim to affect substance use by training pupils how to resist pressure to use, reinforcing attitudes which sustain commitment to continued non-use, and enhancing decision-making, social and life skills. Unplugged particularly emphasised correcting pupils’ beliefs about the pervasiveness of substance use (‘normative beliefs’) by contrasting these with data from surveys of pupils of the same age which typically reveal that average use levels are lower. To make the programme more feasible for schools, it was limited to 12 lessons which can be completed within a school year. The schools’ own teachers taught the lessons after two and a half days’ training in the lessons and materials, and in how to teach them using methods which encourage interaction between pupils and between pupils and teachers, such as role-play and giving and receiving feedback in small groups.
This basic curriculum was supplemented either by meetings led by pupils selected by their classmates, or by workshops for the pupils’ parents. While the curriculum was moderately well implemented, peer-led activities were rarely conducted, few parents attended the workshops, and an important element – role-play – was generally omitted.
Schools were randomly allocated to one of these three variants of the Unplugged intervention or to act as ‘control’ schools which simply carried on with their normal lessons. Taken singly, none of the three variants significantly improved substance outcomes compared to the controls, so reports to date have concentrated on comparing outcomes for all 3547 pupils in the 78 Unplugged schools, to the 3532 pupils in 65 control schools. Excluded from this total were the 27 schools which dropped out of the study after being randomised to the interventions but before their students could be surveyed. Among these were nearly a quarter of the schools allocated to Unplugged. Another five did not conduct the latest follow-up surveys. Of the 7079 pupils surveyed before the lessons, 18 months later (15 months after the Unplugged lessons had ended) 5541 provided usable data at the latest follow-up. In between a a further survey had assessed pupils’ reactions three months after the lessons.
Main findings
At the final follow-up, pupils in Unplugged schools were not significantly less likely to have been drinking or drinking at least weekly (25% v. 30% in control schools) over the past month. However, they were significantly less likely (7% v. 9%) to report having experienced problems related to their drinking over the past year. When the sample was divided up in various ways, this effect remained statistically significant only among pupils not already drinking before the lessons, among those who thought their parents would allow them to drink, and among girls aged 12 or less at the baseline survey.
These results could not include data from the 22% of pupils who did not complete the latest follow-up survey, or who could not be identified as the same individual who completed a baseline survey. On the assumption that they did not change their behaviour or were all non-users, the results remained substantially the same. When instead ‘worst case’ assumptions were applied to each outcome, none were significantly different to those in control schools.
Because (via an anonymous code) individuals could be linked back to their baseline responses, the researchers could identify transitions in substance use patterns and problems. Of the nine possible drinking transitions, just one – non-drinkers becoming frequent (at least weekly) drinkers – was significantly less likely in Unplugged schools, though there was also a tendency for these pupils to more often stay non-drinkers and for occasional drinkers to progress less often to frequent drinking. In respect of drink-related problems, the great majority of pupils had not experienced these before the baseline survey; in Unplugged schools, these pupils were significantly more likely to stay this way and less likely to progress to frequent problems.
The authors’ conclusions
Findings on alcohol-related problems from the featured study together with earlier findings that Unplugged retarded growth in episodes of drunkenness indicate that the curriculum’s preventive effects are limited to problematic drinking rather than the frequency of consumption. Possibly this is because in these European countries, drinking at least to a moderate degree is deeply rooted in and largely determined by culture and society. In contrast, very heavy and problematic drinking is determined more by the individual and their circumstances so is more amenable to educational influences. Based on other findings from the 18-month follow-up, earlier the research team had also concluded that comprehensive social influence curricula can effectively be delivered in the European school setting and help delay onset of substance use, hinder progression to higher levels of use, and facilitate reversion to less intensive patterns of use.
Taking earlier reports together with the current report, it is now clear that the curriculum generally had no significant impacts on substance use, though there were fairly consistent tendencies suggestive of reductions. Specifically, there were no significant impacts on the prevalence of smoking, drinking, or using cannabis or other drugs. Regular use too was generally unaffected, the only significant finding being a short-lived reduction in regular smoking. At a more microscopic level, of 45 possible transitions between use or problem levels, just eight were significantly more or less likely in Unplugged schools, all in a favourable direction. Of these, all but two concerned alcohol. How much these findings can be relied on is questionable. The favourable direction of most other transitions attenuates but does not eliminate concern that among so many tests, some would have thrown up statistically significant differences purely by chance.
The pattern of findings on problem drinking in this report and on drunkenness in an earlier report suggests that the lessons did retard the age-related growth in problem drinking. At the 18-month follow-up, significantly more Unplugged pupils (87% v. 85%) continued to say they had not been drunk in past month, fewer who had been drunk once or twice in the past month at baseline progressed to more frequent drunkenness (16% v. 33%), and more reverted to not being drunk at all (59% v. 39%).
The fact that Unplugged did not significantly reduce alcohol-related problems among pupils who had already drunk or experienced drink-related problems before the lessons may have been due to the small numbers involved. The same cannot be said of the lack of impact among boys or among pupils who thought their parents would not allow them to drink. The latter finding was perhaps indicative of the lessons’ inability to improve on the impact of an anti-drinking culture in the home. However, not too much should be read in to these results. When a sample is subdivided in multiple ways, there is a heightened risk that some differences will be statistically significant purely by chance.
These generally unconvincing results were achieved against a comparator which should have allowed Unplugged to shine. By design, at entry to the study none of the schools were implementing specific drug prevention interventions with strong packages targeted at the relevant school years, a situation which presumably persisted in most control schools. In contrast, Unplugged was intended to be a strong package which could display its advantages in a study large enough to detect these. It seems probable that Unplugged was indeed preferable to doing nothing very much specifically to prevent substance use. However, if this was the case, the benefits were quite limited. Moreover the findings can only be considered applicable to the roughly half of schools prepared to take on the burden of the research and interventions, and to the minority of the entire pupil population taught in such schools who complete the surveys required by research projects. Among schools which did take on the intervention, the parental and peer-leader supplements did not prove feasible and implementation of the core curriculum itself was “just moderate”.
Overall, the findings are not strong enough to alter the view that drug education in secondary schools makes little contribution to the prevention of problems related to drinking and illegal drug use though the evidence in respect of smoking is stronger.
Mixed and generally inconclusive findings of a prevention impact from school programmes targeting substance use do not negate the possibility that general attempts to create schools conducive to healthy development will affect substance use along with other behaviours, nor do they relieve schools of the obligation to educate their pupils on this important aspect of our society. Arguably too, while less or safer substance use may be a desirable side-effect, drug education should be assessed against educational and youth development criteria to do with being relevant and useful as assessed by the young people themselves, rather than pre-set behaviour change objectives.
This draft entry is subject to consultation and correction by the study authors and other experts.

Source: Caria M.P., Faggiano F., Bellocco R. et al.
Journal of Adolescent Health: 2011, 48, p. 182–188.

Filed under: Prevention (Papers) :

HIGH POINT, N.C. — For over three months, police investigated more than 20 dealers operating in this city’s West End neighborhood, where crack cocaine was openly sold on the street and in houses. Police made dozens of undercover buys and videotaped many other drug purchases.
They also did something unusual: they determined the “influentials” in the dealers’ lives — mothers, grandmothers, mentors — and cultivated relationships with them. When police felt they had amassed ironclad legal cases, they did something even more striking: they refrained from arresting most of the suspected dealers.
In a counterintuitive approach, police here are trying to shut down entire drug markets, in part by giving nonviolent suspected drug dealers a second chance. Their strategy combines the “soft” pressure from families and community with the “hard” threat of aggressive, ready-to-go criminal cases. While critics say the strategy is too lenient, it has met with early success and is being tried by other communities afflicted with overt drug markets and the violence they breed.
Overt drug markets — street-corner dealing, drug houses, and the like — constitute one of the worst scourges of poor communities. Such markets foment violent clashes between dealers, as well as robbery by addicts desperate for drug money. Property values suffer. Businesses and families move out — or avoid moving in. Many residents who remain feel under siege. Police often rely on sweeps — mass arrests of street-level dealers — to eradicate drug-related crime. But those rarely provide more than short-term relief. In High Point, police believe that the combination of extensive investigation of the entire market and community involvement has helped solve the problem.
In May 2004, after accumulating evidence in the West End, police chief James Fealy invited 12 suspected dealers to a meeting at the police station, with a promise that they wouldn’t be arrested that night. Encouraged by their “influentials,” nine showed up.
In one room, they met with about 30 clergy, social workers and other community members who confronted them with the harm they were doing, implored them to stop dealing, and offered them help. The suspects, however, “were slouching in their seats and one guy even seemed to be dozing off,” recalls Don Stevenson, pastor of a local congregation, the First Reformed United Church of Christ. “Their attitude was, ‘This is just another program and it will blow over.'”
Then the alleged dealers moved to a second room where they encountered a phalanx of law-enforcement officials: police, a district attorney, an assistant U.S. attorney, and representatives of the federal Drug Enforcement Administration and the Bureau of Alcohol, Tobacco and Firearms, and others. Around the room hung poster-size photos of crack houses that had been the dealers’ headquarters. In front of each alleged dealer was a binder, laying out the evidence against him or her. There were even arrest warrants, lacking only the signature of a judge.
The law-enforcement officials made an ultimatum: stop dealing or go to jail. Several suspected dealers with violent records had already been arrested and were facing maximum charges. The same fate, officials emphasized, awaited anyone in the room who returned to dealing drugs. The district attorney promised to seek the maximum possible sentences, and the assistant U.S. attorney threatened to bring federal charges, which, he stressed, don’t allow for parole. Police from surrounding areas warned them against trying to relocate operations, noting that their names were flagged on statewide law-enforcement computers.
Rev. Stevenson recalls that the alleged dealers “seemed to be paying a lot more attention.”
The West End street drug market closed “overnight” and hasn’t reopened in more than two years, says Chief Fealy, who was “shocked” at the success. High Point police say they have since shut down the city’s two other major street drug markets, using the same strategy.
Police in neighboring Winston-Salem, N.C., as well as Newburgh, N.Y., have deployed the strategy with success, and word is spreading. Encouraged by the National Urban League, which wants to see the approach replicated nationwide, police departments in Tucson, Ariz., Providence, R.I., Kansas City, Mo., and elsewhere are gearing up to try it.
“It’s the hottest thing in drug enforcement,” says Mark A. R. Kleiman, a University of California, Los Angeles professor who specializes in illicit drug issues and isn’t involved in the project.
Some police and prosecutors object to the approach.
“Why not slam ’em from the beginning and forget this foolishness?” says Karen Richards, county prosecutor in the Fort Wayne, Ind., area. The Urban League tried to convince her and the Fort Wayne police to try the strategy, but Ms. Richards didn’t support it. She draws a distinction between addicts, who she believes should get social support, and dealers, who she believes deserve incarceration. “Drug dealers are drug dealers,” she says. “They won’t have an epiphany and end up as model citizens.”
In Winston-Salem, many officers at first dubbed the initiative “hug-a-thug,” though few do so now that they’ve seen it in practice.
In High Point, the West End neighborhood had been a major drug market for almost 15 years, with 16 known crack houses operating at the start of the initiative. A traffic jam began almost every afternoon, as buyers, many destined for homes in the suburbs, converged on the area seeking crack, according to residents and police.
Charlie Simpson, who owns and operates a radiator-repair shop in the West End, says he frequently saw drug dealers “on all four corners, selling drugs out of their pockets.” The dealing drove away business “because women were afraid to come, men didn’t want to bring their wives, plus they didn’t want to leave their car overnight.”
The neighborhood of modest clapboard bungalows became the city’s crime capital. Lucille Dennis, 89, who has lived in the West End for half a century, says that before the initiative, she suffered three break-ins within a year and a half, and she stopped sitting on her porch for fear of getting robbed.
After the West End initiative, violent crime — defined as murder, rape, robbery, aggravated assault, prostitution, sex offenses, and weapons violations — dropped. More than two years later, violent crime remains more than 25% lower in the area, according to police statistics. Since the initiative, there hasn’t been a single murder or rape reported in the West End. “I don’t know exactly how to phrase it,” Mrs. Dennis says, “but you just don’t see as many people riding around doing nothing.”
It isn’t clear how well such an approach would work in big cities, which have much higher absolute numbers of crimes. High Point has about 90,000 residents and Winston-Salem has 190,000. In Kansas City, a city of about 500,000, Police Chief James Corwin says, “Will it work in Kansas City? I don’t really know.” His police department has almost finished the undercover investigation of a drug market it has targeted.
The initiative hasn’t eradicated illegal drug use — and it doesn’t aim to. “This is not a war on drugs,” says Chief Fealy. Rather, he says, the goal is to shut down overt drug markets because “street-level dope-dealing is what drives a significant amount of crime.”
The police had been trying to drive dealers out of the West End for years. “We were actually doing a sting every month in [West End] making dozens of arrests,” says High Point Assistant Police Chief Marty Sumner. “But the market persisted.”
It’s a pattern seen nationwide. In a report published last year by the American Enterprise Institute, authors David Boyum and Peter Reuter point to government statistics that show arrests per dollar of cocaine and heroin sold in the U.S. soared tenfold from 1981 to 2001. Moreover, the percentage of arrests that led to incarceration also shot up; in 2001 more than half the inmates in federal prisons were convicted of drug crimes, up from just 5% in 1981. Yet, during that same two-decade period, the street price of cocaine and heroin, measured in constant dollars, dropped by two-thirds, suggesting it isn’t more difficult to deal. Indeed, the authors estimated that the risk of arrest per individual cocaine sale is less than one in 15,000.
When police do sweep in, Chief Fealy says, they often capture “targets of opportunity” — dealers who are easy to nab. Hardened dealers expect dragnets, so they rarely conduct sales themselves or have significant amounts of drugs in their possession.
Drug dragnets can actually worsen the problem, because some residents resent the heavy-handed tactics, which can inflame racial tensions. Many community members “wonder whose side are the police on,” says Janet Zobel of the National Urban League. Either out of a sense of futility or suspicion, many residents stop cooperating with the police.
The High Point strategy was the brainchild of David Kennedy, a 48-year-old professor at New York’s John Jay College of Criminal Justice. In the 1990s, when he was at Harvard University, Mr. Kennedy helped develop Boston’s anti-gang strategy, a community-involvement approach credited with drastically reducing violent crime.
But the drug initiative was a much harder sell. Mr. Kennedy says he had been trying for more than five years to convince police departments across the country to try it. When Mr. Kennedy first approached Winston-Salem, “We all told him he was crazy,” says Police Chief Patricia Norris. Mr. Kennedy says he would ask, “When do you think what you’re doing now is going to start working?”
Chief Fealy took to the idea the first time he heard it in 2003. He came to High Point from Austin, Texas, where he had been assistant chief and commanded the security detail for then-Gov. George W. Bush.
Before his job interview in High Point, Mr. Fealy drove around the city and was struck by the open drug dealing. “It was just so blatant and in-your-face,” he says. Poring through crime statistics, he saw “well over 60% of our homicides were directly drug-related, and almost 100% of our person-on-person robberies.” He decided to give Mr. Kennedy’s idea a try.
First, police crunch data to find the “hot spots” most plagued by violent and drug-related crime. Then they engage in months of undercover research to understand the local drug market and identify the players — big and small. Police are accustomed to spending months undercover only to nab a major criminal, such as an organized-crime boss. “So putting three months’ work into investigating 20 corner rock dealers” normally would be considered a waste of time, Assistant Chief Sumner says.
But there is a payoff. “A market is something that requires a large number of actors,” says Mr. Reuter, who is an economist as well as an illicit-drugs expert. “If can you can get all the actors out, you can disrupt the system.”
Randy Dejournette, one of the alleged dealers invited to come to the second-chance meeting at the police station in 2004, says “everybody’s gone” from the streets in the West End — and that’s one reason he says he doesn’t deal now. “I’m not going to go out there by myself and sit on the corner and look dumb.”
The High Point police knew who were the lookouts, the runners, the petty dealers and the big wheels. Analyzing the overall market led them to suppliers they might not have found otherwise. Assistant Chief Sumner points to Kevin Cotton, a six-foot-two man with a tattoo that read “thug life,” who was a major source of drugs in a neighborhood targeted by police. An informant told them that he not only supplied dealers, but robbed and intimidated them. He “controlled the market,” Mr. Sumner says. But because he didn’t live in the area, “we probably never would have focused on him.” Police made enough undercover buys to warrant federal charges, then arrested Mr. Cotton because they felt his record was too violent for him to be offered a second chance. He’s now serving 20 years in federal prison.
Arresting violent offenders is one key to making the initiative work. It removes the dominant actors in the market and sets a powerful example. But the other key is that police refrain from arresting suspects who haven’t become hardened, violent criminals. These are often young people — Mr. Dejournette, for example, was 19 when he was invited to the second-chance meeting. For them, police try to implement a communitywide intervention, choreographed to send three clear messages: If they return to dealing, they’ll go to jail; their community will help them turn their lives around but won’t tolerate drug crime any longer; and the police and community are working together to combat dealing.
At the second-chance meeting, police lay out their evidence in a deliberately theatrical way. The Winston-Salem police edited hours of undercover surveillance footage into a short video that showed each suspect making at least one sale. “Raise your hand when you see yourself committing a felony,” the prosecutor told the suspects, according to two people who were there. They started raising their hands, and “that was a thing of beauty,” police captain David Clayton recalls. “They knew we had ’em.”
Alleged dealers are told that they have been put on a special list. “Every one of my assistants has your name,” the district attorney told the suspects at the West End meeting. “And if they don’t prosecute you as aggressively as they can, I’ll fire ’em.” Even the public defender — who would likely represent them in court — warned that the cases were so tight there would be virtually nothing he could do to help them.
Immediate enforcement bolsters that message. The three suspected dealers who didn’t attend the West End community meeting were arrested the next day. One person who attended the meeting but tried to sell drugs days later was also arrested. Police and community groups advertised the arrests by posting fliers throughout the neighborhood with pictures of the suspects.
The threat of going to jail is coupled with a message of support from locals. Jim Summey, pastor of the West End’s English Road Baptist Church and a leader in the community’s anticrime crusade, sums up the message: “We are against what you’re doing, but we’re for you.”
Mr. Dejournette recalls, “We wasn’t expecting that….It did make an impression on me.”
So did something deeply personal: the fact that his mother, Annette Dejournette, was, in her words, “disappointed,” “ashamed” and “hurt” by her son’s actions. She convinced him to attend the meeting even though he had been afraid it was a ploy to arrest him.
Ms. Dejournette works as a clerk in a thrift shop. Money is tight, and often the electricity or phone will get cut off, her son says. “Momma be sitting back crying and stressing, and that make me want to go back outside [on the streets] and really do something to stop my momma from crying, but she the one who talks me out of it.”
The fact that the police are giving nonviolent dealers a second chance has encouraged community cooperation. West End residents have been increasingly calling police to report minor offenses, such as truancy or drunkenness. Ms. Dejournette says she went up to several police officers and city officials and “thanked them for trying to help my son.”
The Winston-Salem neighborhood where the approach was launched last year has proved tougher. The area, centered on the Cleveland Avenue Homes housing project, has fewer community institutions, such as churches, than West End does. Turnover in its public housing is extremely high. Mattie Young, 78, president of the Cleveland Avenue Homes residents’ council for almost 18 years, says the initiative eradicated open drug dealing during the first four months. But since then, she says, it has begun to creep back, especially at night.
Police captain David Clayton says that much of the new dealing may be due to one “very dangerous individual” recently identified by residents, whom police are seeking. Still, comparing the year before the initiative to the year after, major property crimes, such as robbery and burglary, dropped by 35%, according to police figures.
In the three neighborhoods where High Point has implemented the initiative, a total of 40 alleged dealers attended the second-chance meetings. Since then, six have been arrested for dealing. Another 10 have been arrested for various other crimes, from robbery to possession of marijuana. The rest — 24 out of 40 — have stayed clear of the law, police say.
After a dispute with his boss, Mr. Dejournette lost a job with the city parks department. Now, he says, “I fill out applications, but I never get that call back.” He works odd jobs, many through a brother who does construction, but he doesn’t make the $200 a day he says he made running errands for dealers. In April, Mr. Dejournette was arrested but not charged for a nondrug offense, so he is “teetering on the edge,” as Assistant Chief Sumner puts it.
Latisha Fisher, 32, of Winston-Salem, says she had been dealing drugs on and off since she was 15. After going to a community meeting and seeing herself on a police undercover videotape, she took her second chance. Her first job was at a fast-food restaurant. The pay: $6.50 an hour. “I toughed it out” for eight months, she says. “My church and family helped me.” This summer, she landed a job on an assembly line manufacturing earth excavators, making $8.50 per hour.
Yon Weaver, a High Point city employee who helps ex-offenders or suspects find jobs, says only 10 to 15 companies in the area are willing to hire people convicted of a crime. Of the 40 suspected dealers called in to the community meetings, about 10 contacted his office for assistance. He knows three have found jobs. Some suspected dealers have simply dropped out of sight. Police say they don’t think dealers merely relocated, because no new drug hot spots have emerged since High Point’s three markets closed.
Rev. Stevenson says the alleged dealers “are still God’s people, and I want them to do well and have productive, law-abiding lives.” But noting that two murders took place within a block of his church before the initiative, he doesn’t gauge the effort’s success by whether dealers turn their lives around.
“It sounds a little ugly,” he says, “but my first priority is the community.”

By MARK SCHOOFS

Source: WallStreetJournal online. Sept. 27th 2006

By JAN HOLLINGSWORTH The Tampa Tribune
Published: Nov. 12, 2006

The young wrestler was sitting on the kitchen floor, his bloody face illuminated by the early-morning light that streamed through a nearby window. In other parts of the world, the shadow of the moon was edging across the rising sun, marking the beginning of a dramatic and well-publicized total eclipse. Will Hollingsworth had talked of little else for the past four days: the last eclipse of the millennium and the apocalypse some believed would follow. He had not slept in more than 100 hours, holed up in his room, paging restlessly through a Bible, his television tuned to news of the eclipse. It was a peculiar obsession for a 20-year-old college student who spent most of his time training to be a world-class athlete.
Will didn’t appear intoxicated. To the contrary, he was alert, engaging and philosophical, though strangely fixated on current events.

Now this.

On any other day, he would have been out the door — running for miles along eastern Hillsborough County’s busiest roads, pumping iron at the gym, working out with his old high school wrestling team.

But on this August morning in 1999, there was only the inexplicable blood and the vacant stare that greeted me when I came to make breakfast. “What happened?” I asked my only son. “I’ve been fighting demons,” he replied.

Demons?

“It’s true,” he insisted, gesturing to his bloody face and filthy shirt. “I’ve been fighting demons all night. And I won.”

I followed his gaze through the window into the back yard. There, the torn sod and blood-stained patio marked the spot where he had pounded his face into the ground as his father and I slept, oblivious to the war we were about to wage with an invisible enemy. Will would battle his demons for the next three years. But he would never exorcise them. GHB already had laid claim to his sanity, and there was no one who could tell us how to retrieve it.

Dying To Win

Trinka Porrata is all too familiar with the phenomenon of young men who speak of mortal conflict with demons — men who pound their heads on concrete as they experience the unique and little-known psychosis that accompanies GHB withdrawal. “I can’t tell you how many times I’ve heard about that,” said the retired Los Angeles narcotics detective. “Some of them try to put their heads through plate-glass windows.” Some succeed.

Porrata, founder of Project GHB, has spent seven years throwing a lifeline into cyberspace for addicts desperate to escape the grip of a nutritional supplement promoted as a safe, non-habit-forming sleep aid that claimed to build lean muscle mass. Most have been athletes or bodybuilders, but GHB use cuts across all demographics. “It’s the most unique drug,” she said. “We have a lot of senior citizens hooked on it thinking it’s antiaging. It’s big in the gay community, big in the gym scene, big in the club scene. Yet it’s invisible.”

Porrata said she has had more than 1,800 inquiries from GHB users and their family members since Project GHB went online in December 1999. “We were getting: ‘I thought I was the only person in the world with this problem,’” she said.

Before the debut of Project GHB, anyone looking for information on the chemical discovered a nest of Internet sites featuring glowing testimonials, mail-order supplies and recipes for cooking it at home. Central Florida, with its fitness culture, was a watershed for the craze during the 1990s, before GHB-related products were outlawed.

Tampa had its own cottage industry in the form of Body Life Sciences, a now-defunct company that produced and marketed the supplement under the brand names Revivarant and Revivarant G. GHB seemed to offer something for everyone, depending on the dosage: sedation, exhilaration, sexual stimulation, weight loss and the unsubstantiated promise of massive muscles. It was readily available at health food stores and gyms, where it entered the marketplace as an ostensibly safe, legal alternative to steroids.

In recent years, its ability to induce mild euphoria and amnesia attracted a new kind of customer who employed it as a party drug associated with overdoses and sexual assaults. GHB’s link to “date rapes” and all-night raves quickly overshadowed its widespread use in the athletic community. Yet it is the athletes and bodybuilders, who incorporate it into a daily regimen, who are most at risk of becoming addicted.

“It’s really the frequency of the dose as opposed to the amount of the dose that leads to this very striking psychosis,” said David Kershaw, a psychologist for Hillsborough County’s Mobile Crisis Unit. Kershaw has seen his share of GHB addicts in withdrawal — beginning in late 1999, when the county’s mental health center saw a rash of cases involving muscular young men suffering from hallucinations and paranoia.

One believed he had an invisible tape recorder fastened to his leg. Another saw a swarm of flies covering his body. All were regular users of GHB. “The irony is that despite the fact that they wouldn’t deliberately pollute their bodies like that, they get sucked into using it,” Kershaw said. “The people I see are all athletes, all concerned with being as healthy as they can be.”

One of them was Will.

The Runner Stumbles

Will’s descent into madness was swift and seemingly irreversible.

The first sign that something was amiss came one night in the spring of 1999, when he called to ask his father to come help him change a flat tire. It turned out the tire was flat because Will had drifted off an exit ramp on Interstate 75 and into a tree. Weeks later, another late-night call — this one from an ex-girlfriend, who said she had received an urgent message from Will asking her to pick him up at a gas station near the University of South Florida.

When she arrived, she found the car, with the engine still running, the driver’s door ajar, but no sign of Will. He turned up at another nearby gas station — incoherent, with no memory of how he got there. His father and I were mystified. Will seemed as bewildered as we were. “I keep making mistakes, and I don’t know why,” he said.

He never made the connection between the potion he bought at the local health food store and the bizarre things that happened when he stopped using it. We didn’t know he was using GHB. There were a lot of things we didn’t know.

The Will we knew was exceptionally bright, responsible, hardworking and honest. A good student, a loyal friend and — most striking — a gifted athlete with a passionate dream to be the best of the best — at something.

He was, at one time, the fastest boy in Hillsborough County — sprinting and jumping his way through a medley of track-and-field titles during his middle school years. There was a charisma about the sturdy blond boy whose blistering speed brought stadium crowds to their feet as he entered the homestretch.

When he earned a place on the Brandon High School wrestling team — one of the premiere prep athletic programs in the nation — he told a sports reporter what it meant to soar with the Eagles. “I feel there is no limit to where I can go,” he said in a 1997 newspaper interview. “It is a great team and I don’t think my life will ever be the same.”

Death And Detox

About the time the young wrestler was beginning to unravel in Florida, bodybuilder Mike Scarcella, a former Mr. America, was arrested in Texas, charged with felony possession with intent to distribute GHB.

The U.S. Food and Drug Administration had banned the supplement in 1990 but left loopholes that allowed its analogues — chemical cousins that turn into GHB after ingestion — to be sold for another decade. By all accounts, including his own, Scarcella had been using the supplement for years — first as a muscle-building nightcap, then as a morning pick-me-up. Eventually he was sipping capfuls throughout the day, a classic pattern among athletic users that can lead to physical dependence in a matter of weeks or months. Scarcella was hooked. His May 1999 arrest, which resulted in 10 years’ probation, was not enough to pry him from the grip of GHB.

The 1992 Mr. America continued to use and sell the drug, even as he tried to kick the habit — first on his own, then in hospitals, where doctors had no experience with the bizarre hallucinations and raging psychosis of GHB withdrawal.

Even with a doctor’s help, withdrawal can be deadly. Stroke, heart attack and suicide are among the consequences for addicts in withdrawal, which can start within one to three hours of a missed dose.

Anxiety, restlessness and insomnia can quickly progress to delirium, muscle tremors and delusions.

“They think they’re on fire. They’re moving, thrashing, screaming,” said Karen Miotto, a University of California-Los Angeles addiction psychiatrist who helped develop a GHB detox protocol. “I think GHB is probably harder to get addicted to than some other drugs,” she added. “But once people get addicted, it is far harder to get off than any drug I’ve seen.”

Scarcella’s battle ended in August 2003, when the 39-year-old bodybuilder was admitted to a Texas hospital feeling the first effects of GHB withdrawal. By the 10th day, he had become delusional and suffered what the medical examiner termed “sudden cardiac death.”

Doctors and psychiatrists have been slow to recognize GHB withdrawal. Most know little beyond its reputation as a date-rape or club drug with the potential to deliver a swift, deadly knockout punch. Emergency room physicians have become familiar with the unconscious overdose patients — generally youthful partiers — who are often treated and released.

But they rarely consider GHB use in the muscular, hallucinating patients who are delivered in four-point restraints. “ER doctors don’t really know what to look for,” Kershaw said. Most physicians and mental health professionals also fail to recognize the early stages of withdrawal, when careful detoxification using the right medications might head off a spiral into psychosis. “It really means that the only time they’re going to get help is when they’ve reached the state of hallucinating,” said San Francisco addiction specialist Alex Stalcup. By then, their condition may be far less treatable.
“It’s just heartbreaking.”

Jesus’ Son

The angels appeared in September 1999, shortly after the eclipse that marked the end of life as we knew it.
These were not benevolent guardians, but mute, shadowy creatures only Will could see. What was their purpose? I asked him. “They’re here to watch us,” he said. Not as protectors but observers. They were neither dangerous nor benign. They just WERE, he said. Six weeks had passed since the morning of Will’s bloody battle with the backyard demons.

His father and I had spent the first week taking turns staying home from work with him as he slept round-the-clock, sedated by a physician.

The sleep deprivation that preceded the incident was enough to cause hallucinations, according to a psychologist friend. Perhaps sleep would bring him out of it, she suggested. We knew by this time that GHB had played some role. Will had acknowledged taking the supplement in the week before the eclipse. But he had stopped about three days before, he insisted. When Will finally woke up by week’s end, the crisis seemed to have passed.

He returned to his part-time job as a waiter at a Brandon restaurant and began his junior year at USF. With his sights set on the Olympics since high school, he resumed his regular workouts — and, according to his off-campus roommates, resumed his GHB use. “It takes you to a place you never want to come back from,” Will said.

On Labor Day, he was back home, reading the Bible around the clock. He stopped attending classes, didn’t report for work and did not return to the apartment he shared with three other students. He had stopped taking GHB.
He also had ceased his workouts and stopped eating. He claimed he was going to fast for two weeks — “like Jesus.”

Once again, his father and I took turns working from home, watching, waiting. He was, by law, an adult and could not be forced into an evaluation unless he proved to be a danger to himself or others. He didn’t meet that criterion — not yet. His father took his car keys, just in case. Sept. 17, 1999. It was my turn to watch over Will.

I worked on a news story from my laptop on the dining room table, just outside his bedroom. Each time I checked on him, he was sitting on his couch, reading his Bible. He had not eaten since Sept. 6. Shortly before 6 p.m., Will wandered out of his room and pulled up a chair across from me. My fingers froze on the keyboard as I met his gaze. “What are you working on?” he asked. I knew he couldn’t possibly be interested, but it was the first time in weeks he had made any effort to engage in conversation. I began to explain the story I was writing. Then I saw it, so plainly that for a moment I thought I was the one losing touch with reality.

Will’s gray-green eyes, the windows to his troubled soul, suddenly transformed into black pools of blazing madness. And for the first time, I understood the concept of possession. I was still answering his question when he cut me off in midsentence. “You don’t know who you’re dealing with, do you?” hissed the suddenly dark, dangerous creature.

“No,” I replied, cautiously. “Who AM I dealing with?” He rose from his chair and took a step toward me, his fist clenched, his face contorted with rage. “I am the Lord Jesus Christ, and I want my car keys.” I glanced at the clock. His father was due home any time now.

Will’s lips smiled, but his eyes still glittered with that dark madness. “He’s not going to save you,” he said, as though he had read my mind. The phone rang. Will answered. “Yeah, Dad. She’s right here,” he said, handing me the phone, still smiling that frightening smile. Whatever I had seen in Will’s eyes, his father heard in his voice. “Can you talk?” he asked me. “No.”

“Something is wrong?”

“Yes.”

“Get out of the house,” Will’s father told me. “Get out NOW.” Clearly the time for watching and waiting was over. His father dialed 9-1-1.

That night, the angels made their first appearance as Kershaw and his mobile crisis unit came to commit Will for 72 hours of psychiatric observation under Florida’s Baker Act — the first of nearly a dozen hospitalizations over the next 30 months. It wasn’t a tough call. Will was in “florid psychosis” and claimed alternately to be God, Jesus and Jesus’ son.

Then there were the angels, who would, in time, become Will’s constant companions. Kershaw was among the few professionals we encountered over three years who took serious note when we told him of the GHB link.

“Will’s case prompted me to educate myself on this,” he said. “If I have someone who’s got psychotic symptoms, and they’ve got a history of being a fairly well-functioning athlete with no history of mental illness, one of the first things I think of now is GHB.”

Spontaneous Combustion

GHB was the last thing David Johnson thought of as he searched the Internet for information about “Enliven,” a supplement his 28-year-old son, Tyler, purchased at a health food store near his home in Beebe, Ark.

Tyler, who had graduated weeks before from the University of Arkansas, became restless and “fidgety” on the night of July 15, 2000. His pulse raced, and he began to say things that didn’t make sense, Johnson said. Unknown to Johnson, the young bodybuilder had been taking Enliven for about a year. Now, engaged to be married and about to begin law school, Tyler had decided to stop taking it. That night, he showed his father a bottle of the supplement, labeled as a “100% Pure Cellular Recovery System” that “Renews the Body Naturally.”

What it didn’t say was the active ingredient — 1,4 butanediol, better known as BD — is a solvent that converts into GHB once ingested.

GETTING OFF ‘G’
Withdrawal from GHB is among the most prolonged and severe of any drug and should not be undertaken without medical supervision.

Cardiovascular distress is significant, posing the risk of stroke or heart attack. Spikes in blood pressure from repeated bouts of withdrawal can result in arterial damage and an enlarged heart. Withdrawal grows more severe with each subsequent attempt, “kindling” the nervous system to the point of inducing delirium or seizures.

Patients treated before they reach this stage stand a better chance of successful recovery. Detox begun in early stages of withdrawal, with onset of restlessness and anxiety, works best. Detox generally takes at least two weeks, often requiring heavy doses of sedatives, accompanied by monitoring of blood oxygen levels. David Johnson didn’t know it, but Tyler was in GHB withdrawal.

“I wanted to take him to the hospital, but he told me he was all right and he went to bed,” Johnson said.

The next morning, shortly after dawn, a neighbor discovered Tyler’s body on the Johnsons’ front lawn. He had shot himself in the head. Suicide is an all-too-common outcome in cases of GHB addiction, though the true numbers will never be known. Porrata has seen it over and over.

“It’s like spontaneous combustion, not like they pondered it. They just shoot themselves in the head,” she said.
Detox from GHB can take at least two weeks.

“I think one of the most dangerous periods is after detox, where they are suffering depression, anxiety, and it becomes this protracted withdrawal state,” Miotto said. GHB anxiety is malignant — the frightening dreams at night, the terror during the day as the central nervous system tries to deal with the legacy of a little-understood chemical assault on the brain, Stalcup said. “If I had to go through what I see people going through, I don’t know if I could do it,” he said.

Perhaps the harshest irony, Porrata said, is the people who become addicted to GHB in the pursuit of health and fitness and end up turning to street drugs to counter the effects of withdrawal. Black-market Xanax, Valium and similar drugs tend to be the ones of choice. Alcohol, cocaine, Ecstasy and even crystal methamphetamine aren’t far behind.

Of Dreams And Nightmares

In the weeks and months that followed Will’s first Baker Act, life took on a rhythm of sorts — but not the sort we envisioned.

By day, Will continued to run, lift weights, wrestle and pursue his athletic dreams. By night, he battled the demons that invaded his sleep. The boy who once was a designated driver for friends retreated to his room, alone, to drown the delusions in rum and vodka.His circle of friends shifted from students and athletes to dropouts and drug dealers who could ensure a steady supply of sedatives and anything else that might quiet the voices and visions.

I purchased a dreamcatcher and hung it beside his bed, hoping the mystical Indian legend would offer some comfort.

But nothing could banish the nightmarish images that appeared when he closed his eyes. “You can’t imagine what is happening in the world,” he told me. “Yes, I can.” I had to look no further than the gaping hole in his soul.

Laced with antipsychotics prescribed by his doctors, supplemented by a pharmacopia of his own invention, Will struggled to hold down a job and tried, unsuccessfully, to complete his junior year.

He teetered for months on the brink of madness, alternately stabilizing, then disintegrating into a series of forced hospital stays. We didn’t know whether he continued to use GHB or whether the drug had permanently rewired his brain.

“With Will, when I saw him again and again, I wasn’t sure if the GHB had triggered more of a chronic process with him,” Kershaw said. Each time Will was committed, we asked the nurses and doctors to flag his chart to reflect his GHB use — a request that often was received with blank stares and dismissive waves. Will continued to slip from our grasp, trapped in a world inhabited by demons and angels, a world defined by the absence of light or joy.

We wondered how long he could survive in such a dark and hopeless place. It didn’t help that he had come to believe he possessed the gift of prophesy and claimed to have seen his own death many times. He wouldn’t tell us when this was to occur. All he would say was that it involved fire.

Drowning In Cases

In the beginning, the addicts who flocked to Project GHB for help tended to be young men in their late teens and early 20s. Today, Porrata is seeing older men who have been using for five to 10 years. Most are 30 to 55 years old.
“It’s not the party kids,” she said. “It’s the man in midlife crisis who starts going to the gym and wants to lose a few pounds, look a little better, rekindle things — and someone introduces him to ‘G.’”

But still it is the athletes who concern her the most. “Any place you see steroids, GHB is right in the shadows,” she said. “The sports world won’t admit this drug. It’s like their secret drug, and they won’t give it up.”

Unlike steroids, there is no evidence GHB enhances physique or performance. Still, users subscribe to the myth.

“What makes GHB so attractive to athletes is it’s very difficult to detect. They pass all the routine urine drug screens that you do,” said Tampa addiction specialist David Myers.

One of Myers’ patients — a Major League Baseball player — sipped GHB from a small mouthwash bottle during his games. He told Myers and his team managers that GHB use was widespread in pro sports, including among his teammates.

“He relapsed,” Myers said. “There was no support from team management, and it was clear they were not interested in tackling GHB issues.”

There is some speculation that stepped-up enforcement has limited the drug’s availability. But despite a major Drug Enforcement Administration sting that netted 115 Internet distributors in 84 North American cities in 2002, followed by a $7 million bust this year in Scotland, there is plenty of GHB to go around. With Project GHB and other Internet sources supplying information that wasn’t available to addicts six years ago, many users are taking matters into their own hands, Porrata said. “They’ll die from other drugs,” she said. “And we’ve had so many suicides — so many.”

The Three Demons

Will’s final Baker Act took place Jan. 18, 2002. His slide into psychosis began as it always did: He stopped eating.

This time he said he planned to fast until Easter. When he entered Memorial Hospital’s psychiatric unit that day, he had been fasting for two weeks and had lost nearly 30 pounds. A public defender assigned to Will’s case blocked every effort to give him intravenous fluids and nutrients. If he wanted to starve himself, it wasn’t our business, or his doctor’s, she said. By February, Will was still fasting and began walking into walls. He fell and hit his head.

Then something remarkable happened: After three years of inexplicable madness, someone finally decided to take a look at Will’s brain. A nurse requested a CT scan. It was then that we finally met his demons. There were three of them: inoperable brain lesions whose nature and origin doctor’s couldn’t even guess at. Will was transferred to the medical floor, and for the first time in nearly two months, he received IV fluids and nutrients. Too late.

The neurological collapse began with involuntary flickering of his eyelids, which grew more pronounced each day. His hearing began to fail. He started to lose the use of the right side of his body. Still he would not eat. “Don’t worry,” he said. “I’ll be fine.” “All you have to do is start eating, and they’ll let you out of here,” I pleaded. “Isn’t there someplace you’d rather be?” “Heaven,” he said. On Easter, Will broke his fast with a Cadbury egg. He was transferred to a physical therapy unit, then sent home.

The brain scan was sent to Johns Hopkins University in an attempt to identify the lesions. The young wrestler, once the fastest boy in Hillsborough County, could not get from the bedroom to the bathroom without a walker. His balance was gone, his hearing severely impaired. And his flickering eyes couldn’t focus on a television screen, much less a Bible.
But he could kneel, and he could pray. And that is what Will did each day. “Everything will be fine,” he kept saying. “I’ve seen the future, and I’ll be wrestling.”

One of the saddest things about GHB, Miotto said, is the way the drug affects the mind. “They don’t grasp the level of their impairment,” she said. But the saddest thing about Will’s experience was his ability to grasp just that.

Despite his irretrievably broken mind, he knew what he had lost. He knew it all along. Will had always felt a particular affinity for the homeless. In the years he struggled with GHB psychosis, he actively sought them out to give them money as they picked through garbage bins. “That could be me someday,” he said. Despite his intermittent delusions of grandeur, his goals were humble. “What do you want from life?” I asked him shortly before that last Baker Act.

“I just want to be able to take care of myself,” he said. “To drive a car. To have a place of my own.”
Weeks after Will’s release from the hospital, his doctor evaluated him. He checked his eyes, his ears, his balance. This, he told him, was as good as it was going to get. As for the three still-unidentified brain lesions — things could get worse, he added.

Four days later, on June 3, 2002, my son took a gas can from the garage to the back yard. He doused himself and lit a match. A young man approached me after the memorial service. He said his name was Brandon and that Will had persuaded him to seek treatment for cocaine addiction.

“I’m two years clean and sober now,” he said. “Will saved my life, and I just wanted you to know.”

Source: Researcher Mike Messano contributed to this project. Reporter Jan Hollingsworth can be reached at (813) 865-4436 or jhollingsworth@tampatrib.com.

PRODUCT NAMES

Blue Nitro
Renewtrient
Revivarant
Remforce
Firewater
Enliven
Serenity
Revitalize Plus
Thunder Nectar
Rejoov
Flower Power
Dream On
Weight Belt Cleaner

Source: Project GHB

Filed under: Social Affairs (Papers) :

There can be few ideas that have been more immediately appealing than reducing the harm associated with the use of illegal drugs. When it was first articulated in 1988 by the Advisory Council on the Misuse of Drugs harm reduction offered those in the drugs field a way of engaging with clients in which there were more gains, more easily achieved, than the often slow progress of the long road to recovery from dependent drug use.

It is impossible to calculate the amount of money that has been directed at harm reduction within the UK over even the last fifteen years but that figure must be in the tens of billions of pounds. Methadone maintenance, a cornerstone of harm reduction influenced drug treatment, has consistently absorbed the lion’s share of what is now an £800 million a year treatment budget. Hundreds of millions of needles and syringes have been given out to injecting drug users and thousands upon thousands of drug users have been counselled in the practices of safer drug use.

The position of harm reduction at the very forefront of UK drug treatment policy is looking much less assured today than at any time in the recent past. The current drug strategy contains only a single, passing reference to the term (and even that is only a footnote to the alcohol harm reduction strategy for England). The pre-eminent focus of the UK drug strategy is on the recovery rather than simply reducing the harms associated with individual’s drug use (HM Government 2010). So why has harm reduction fallen so far from its favoured position?

First, harm reduction may have suffered as a result of the sheer success it has enjoyed in attracting massive government support set against the evidence of continuing and in some respects escalating drug harm. Hepatitis C is now so widespread amongst injecting drug users that it is difficult to see how, in the absence of harm reduction measures, it could be any more prevalent. In some cities 60% of injecting drug users are Hepatitis C positive. Drug related deaths have continued at an intolerably high level (around 2000 a year) despite a government commitment to reduce the numbers of addict deaths. In some cities, most notably Edinburgh, there have been more deaths associated with methadone than with heroin. There are signs that the level of HIV infection amongst injecting drug users long championed as a success of harm reduction is starting to increase. Between 60% to 70% of crime is connected to the drugs trade and there are clear indications of children using drugs at an increasingly young age. We are now seeing a cocaine problem that has already overtaken our heroin problem. We estimate that there are around 400,000 children growing up with one or both parents dependent upon illegal drugs. None of these are the statistics of a drug problem whose harms have been effectively reduced. The persistence of those harms has given rise to a growing feeling that it may only be by reducing the overall level of drug use that it will truly be possible to reduce the extent of the drug harms we are seeing.

Second, political support for harm reduction may have waned in the face of the evidence that most drug users entering treatment are looking not for advice on how to use their drugs with lower levels of harm but for support in how to become drug free. The first research paper reporting that finding came from Scotland showing that approaching sixty percent of drug users starting a new episode of drug treatment were looking for help in achieving a single goal – to become drug free (McKeganey et al 2004). Those findings were initially rejected by many in the drugs field although a large, National Treatment Agency survey in 2007 reported that 80% of drug users in treatment who were those using heroin, 73% of those using crack cocaine, and 50% of those on methadone were seeking to become drug free (National Treatment Agency, 2008). The emphasis on abstinence in these studies ought not really to have threatened the harm reduction lobby since abstinence was very much at the heart of the earliest formulations of the harm reduction approach. The Advisory Council on the Misuse of Drugs “Act AIDS and Drug Misuse Report”, for example, set out a hierarchy of goals which combined the aim of reducing the shared use of injecting equipment with the aims of reducing the use of prescribed drugs, and increasing abstinence from all drug use. Over time however, harm reductionists steadily diluted their commitment to reducing all forms of drug use (McKeganey 2011).

Third, political support from harm reduction may have waned as a result of the increasingly strident tone of some harm reductionists lobbying in support of the drug using lifestyle and calling for some form of relaxation in the drug laws. Levine has written that “harm reduction is a movement within drug prohibition that shifts drug polices from the criminalized and punitive end to the more decriminalized and openly regulated end of the drug policy continuum. Harm reduction is the name of the movement within drug prohibition that in effect (though not always in intent) moves drug policies away from punishment, coercion, and repression, and toward tolerance, regulation and public health”. (Levine 2001). Craig Reinarman, a U.S. academic supportive of harm reduction has identified the dangers of an increasingly strident tone on the part of some harm reductionists in calling for drug law reform. “The (harm reduction) movement has succeeded”, Reinarman writes, “partly because it blended human right and public health, not because it chose one as superordinate.…The public health principles that under gird harm reduction practices have afforded much needed political legitimacy to controversial policies. This legitimacy is a precious resource, some of which might be jeopardized if the movement were to give loud primacy to the right to use whatever drugs one desires and to make legalization its principle policy objective” (Reinarman 2004:240)

UK drug policy is now at an intersection in which one of the key questions that needs to be addressed has to do with whether it will be possible to combine the current focus on recovery with a commitment to continue to support services aimed at reducing drug related harm. Those who have benefited from the allocation of substantial public funding for harm reduction initiatives may well see their budgets reduced as resources are targeted on the recovery focussed services. If the reaction to any such rebalancing of the drugs treatment budget is an increasingly belligerent tone on the part of those who support harm reduction, it is questionable whether such a combination will be able to develop (Stimson 2010). However, successful interlinking of these approaches may also require harm reductionists to temper their support for drug law reform, emphasising less the rights of the individual to use illegal drugs, and concentrating rather more on individual and public health protection.
Neil McKeganey, Professor of Drug Misuse Research University of Glasgow

Source: Wither Harm Reduction? : UK Drink & Drug News February 2011

References
Advisory Council on the Misuse of Drugs (1988) AIDS and Drug Misuse: part 1. London: HMSO, 1988.

HM Government (2010) Drug Strategy Reducing Demand Restricting Supply Building Recovery: Supporting people to live a Drug Free life

Levine, Harry G. (2001), The secret of world-wide drug prohibition: The varieties and uses of drug prohibition. Hereinstead , October 2001 On-line: .

McKeganey, N., Morris, Z., Neale, J., Robertson, M. (2004) What are drug users looking for when the contact drug services Abstinence or harm reduction Drugs Education Prevention and Policy 11 (5) 423-435

McKeganey, N (2011) Controversies in Drugs Policy and Practice. Palgrave

National Treatment Agency (2008) 2007 User Satisfaction Survey of Tier 2 and 3 Service Users in England.

Reinarman, C. (2004) Public Health and Human Rights: The virtues of ambiguity International Journal of Drug Policy 15 pp 239-241.

Stimson, G, (2010) Harm reduction: the advocacy of science and the science of advocacy The 1st Alison Chesney and Eddie Killoran Memorial Lecture. London School of Hygiene and Tropical Medicine 17th November 2010

“The science is finally in on the link between cannabis use and early onset psychosis. New Australian research has provided the first conclusive evidence that smoking cannabis hastens the appearance of
psychotic illnesses by up to three years….The risks are especially high for young people whose brains are still developing.”

So were the opening lines of ABC Radios Tony Eastley’s AM report on the latest Australian research into Cannabis and psychosis. The study was carried out on an incredibly large sample group and drew on research from scores of international studies.
However, will this report, one in a long line of scientific and ‘evidence based’ papers, actually be embraced or will it be swept away (as many others have) by the relentless and often unchecked rhetoric of the shameless pro-drug lobby and their spin ‘doctors’? One of the most manipulative terms used in the pro-legalisation platform is ‘evidence based science’
and of course such ‘science’ is rarely geared to the detrimental social, familial or long term physical or mental health of individuals; no, it is aimed at trying to convince the understandably unaware public, that drug use and particularly cannabis use, isn’t a problem. It is posited by such peddlers that only ‘problematic drug use’ that may be the problem and that ‘science’ is there to help us manage the problem, not prevent it.

These most recent findings are by no means new. In recent years Professor Jim van Os and his team at the Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network in the Netherlands in another significant study into cannabis and youth psychosis concluded the following…
“Cannabis use … increases the risk of psychotic symptoms in young people but has a much stronger effect in those with evidence of predisposition for psychosis.”2
The publishing on line in the last few days, of findings from researchers at NSW Prince of Wales hospital concluded that:

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.3

Yet again, this is not new, other previous and standing research as also found…
It has also been argued that 27% of the population carry a high risk genetic variant which produces a weaker Catechol-O-Methyl Transferase (COMT) enzyme which is responsible for the breakdown of dopamine in the brain…those cannabis users with weaker COMT enzyme are at 10 times greater risk of developing psychosis and,
later in life, of developing schizophrenia…the greater the amount of cannabis consumed correlates to a higher degree of risk of psychosis4

The potential damage of this cannabis induced psychosis was no more apparent than in the recent Tucson massacre at the hands of Jared Lee Loughner. In a commentary from the Institute for Behaviour and Health titled Marijuana, Schizophrenia
and Jared Loughner the following was revealed….
‘Overlooked by most commentators is Loughner’s history of heavy marijuana and alcohol use… Loughner has a serious mental disorder, probably paranoid schizophrenia…One important message that must be heard amidst the chatter over this tragedy is that marijuana is not a harmless recreational drug. The sale and use of marijuana is often trivialized, or even glamorized. Marijuana use is neither trivial nor glamorous. Marijuana use is linked to addiction, to dropping out of high school, to lower educational attainment, to other substance use, and to mental illness. Marijuana use doubles the risk and hastens the onset of schizophrenia. Once schizophrenia emerges, marijuana use adversely impacts the course of the disease. Schizophrenics are about twice as likely to smoke marijuana as individuals without this mental disorder. Marijuana use not only makes the symptoms of this disease
worse, but it reduces the effectiveness of treatments for schizophrenia. Marijuana use predicts an increase in the severity of psychotic symptoms.5

These evidences should be enough in and of themselves to renew efforts to diminish and not promote this pernicious substance, but this is only one of the health risks that Cannabis presents. What is important to note is that this illicit substance, touted as harmless to ‘most’ couldn’t be further from that, and its impact is not
restricted to mental health arena, but can and does inflict serious harm to users as the following outlines…

There is evidence of psychiatric, respiratory, cardiovascular, and bone toxicity associated with chronic cannabis use. Cannabis has now been implicated in the etiology of many major long-term psychiatric conditions including depression, anxiety, psychosis, bipolar disorder, and an amotivational state. Respiratory conditions linked with cannabis include reduced lung density, lung cysts, and chronic bronchitis.
Cannabis has been linked in a dose-dependent manner with elevated rates of myocardial infarction and cardiac arrhythmias. It is known to affect bone metabolism and also has teratogenic effects on the developing brain following perinatal exposure. Cannabis has been linked to cancers at eight sites, including children after in utero
maternal exposure, and multiple molecular pathways to oncogenesis exist.

Conclusion
Chronic cannabis use is associated with psychiatric, respiratory, cardiovascular, and bone effects. It also has oncogenic, teratogenic, and mutagenic effects all of which depend upon dose and duration of use.6

It is time that responsible and health conscious Australians, particularly policy formulators and legislators take head to the scientific evidence that refutes the manipulative rhetoric of a few, if not malevolent, then staggeringly naïve activists; those who seek only to promote the ‘rights’ of a dysfunctional minority at the expense of the mental, social and physical
health of an entire generation. It’s time to prevent, not promote!

Source: www.dalgarnoinstitute.org.au www.nobrainer.org.au Feb.2011

Endnotes
1 http://www.abc.net.au/am/content/2011/s3132596.htm 2/8/2011
2 Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people Cécile Henquet, Lydia
Krabbendam, Janneke Spauwen, Charles Kaplan, Roselind Lieb, Hans-Ulrich Wittchen, Jim van Os (Paper for BMJ Online First bmj.com)
3 Cannabis Use and Earlier Onset of Psychosis A Systematic Meta-analysis Matthew Large, BSc(Med), MBBS, FRANZCP; Swapnil Sharma, MBBS,
FRANZCP; Michael T. Compton, MD, MPH; Tim Slade, PhD; Olav Nielssen, MBBS, MCrim, FRANZCP Arch Gen Psychiatry. Published online February 7,
2011. doi:10.1001/archgenpsychiatry.2011.5
4”Cannabis – suicide, schizophrenia and other ill effects: a research paper on the consequences of acute and chronic cannabis use.” Drug Free Australia March 2009
5 Marijuana, Schizophrenia and Jared Loughner – Commentary; Institute for Behaviour and Health (Jan 2011)
6 ‘Chronic toxicology of cannabis Dr. ALBERT STUART REECE Medical School, University of Queensland, Highgate Hill, Brisbane, QLD, Australia –
Clinical Toxicology (2009) 47, 517–524 Copyright © Informa UK, Ltd. ISSN: 1556-3650 print / 1556-9519 online DOI: 10.1080/15563650903074507
LCLT REVIEW Cannabis toxicology (taken from Introduction summary)

In 1996 a ballot initiative in California was approved (Prop. 215, and its successor SB420), which allowed for a smoked (!) leaf of unknown chemical composition, unregulated doses of psychoactive ingredients and hundreds of other potentially hazardous chemicals, to treat serious medical conditions, including “AIDS, anorexia, arthritis, cachexia, cancer, chronic pain, glaucoma, migraine, persistent muscle spasms, seizures, epilepsy, severe nausea, any other chronic or persistent medical symptom that substantially limits the ability of the person to conduct major life activities”. Prop 215 passage had nation-wide ramifications and set off a cascade of ballot initiatives in other states, including Montana.

A. MARIJUANA AS MEDICINE

1. The most obvious objection to Prop 215 is the use of smoking as a delivery system for drugs, after a 40 year national campaign to end smoking.
2. The second objection is the poor quality or no evidence for marijuana’s safety and efficacy in treating a myriad of diseases listed in the ballot initiatives

A few years after Prop 215 passed in California, Governor G. Davis funnelled millions of dollars into medical marijuana research, to seek validation, after the fact, for these “ballot-approved” medical claims. After a decade of funding, this California Center for Medicinal Cannabis Research has issued 24 publications.
Only 3/24 reports focus specifically on clinical studies to examine the effectiveness of marijuana in treating diseases listed in the ballot initiative. Only one medical condition is explored, neuropathic pain in AIDS patients. Intriguingly, recruited subjects were required to be experienced marijuana smokers and all subjects were maintained on other painkillers, but the manuscripts do not report any details on other painkillers. In the majority of observational studies published on the “therapeutic” effects of smoked marijuana, there is no reporting of side effects (e.g. intoxication, cognitive impairment, etc), information that the FDA considers essential for FDA approval. These include whether marijuana produced a feeling of “high” (“euphoria”), being impaired, feeling sedated and showing cognitive impairment in objective tests of learning, speed recall, attention.

As for the other medical indications for marijuana, five major clinical trials were discontinued because the investigators could not recruit enough patients, despite extensive advertising, to study marijuana effectiveness for relief of cancer pain, muscle spasticity, multiple sclerosis, severe nausea and vomiting, neuropathic pain. The intent to investigate was present, but candidate patients refused to enroll. It raises significant questions as to why 16 of the remaining research projects did not address the core reason for the state funding, whether marijuana is effective in all the medical conditions and indications specified in 215 and SB420.
3. The third objection, of national significance, is that ballot initiatives circumvent stringent Federal FDA standards, a direct threat and challenge toour elaborate, technical- and evidence-based, national drug approval system. FDA standards have protected Americans from fraudulent, dangerous or ineffective drugs for decades, with an approval system, although imperfect, that is among the most rigorous in the world. Consider the wise FDA response to ballot initiatives for the sham cancer treatment laetrile, their denial of thalidomide approval and a myriad of other drugs deemed unsafe and unacceptable by rigorous standards. Circumvention of FDA approval by a ballot initiative is a dangerous precedent, a slippery slope that can create chaos in the evidence-based approval process for medicines.

B. FDA REQUIREMENTS

The FDA requires that a drug:
a. is a pure compound
b. its chemistry, manufacturing, and composition of matter are tightly
controlled so that each batch is identical
c. its production methods are validated
d. its shelf life is known and can be dated to protect patients from a degraded chemical
e. its microbiology is known (batches of chemicals contaminated with bacteria are rejected)
f. its pharmacology and toxicology in animals is known
g. its rate of entry, bioavailability, toxicology are known
h. its dose response, efficacy, safety are known
i. its side effect profile is documented.
j. after approval, requires case reports and safety updates to be submitted to the FDA for ongoing evaluation.

Ballot initiatives for alleged treatments erode this carefully constructed process and lead to compromised quality of our nation’s medications.
The FDA ruling on marijuana as medicine is given below. It has not changed. Marijuana is listed in schedule I of the Controlled Substances Act (CSA), the most restrictive schedule.

• The Drug Enforcement Administration (DEA), which administers the CSA, continues to support that placement and FDA concurred because marijuana met the three criteria for placement in Schedule I under 21 U.S.C. 812(b)(1)
• Marijuana has a high potential for abuse has no currently accepted medical use in treatment in the United States
• Lacks accepted safety for use under medical supervision.
• There is sound evidence that smoked marijuana is harmful.
• A past evaluation by HHS agencies, FDA, SAMHSA and NIDA, concluded that no sound scientific studies      supported medical use of marijuana for treatment in the United States
• No animal or human data supported the safety or efficacy of marijuana for general medical use.
• There are alternative FDA-approved medications in existence for treatment of many of the proposed uses of smoked marijuana
• A growing number of states have passed voter referenda (or legislative actions) making smoked marijuana available for a variety of medical conditions upon a doctor’s recommendation.
• These measures are inconsistent with efforts to ensure that medications undergo the rigorous scientific scrutiny of the FDA approval process and are proven safe and effective under the standards of the FD&C Act.
• Accordingly, FDA, as the federal agency responsible for reviewing the safety and efficacy of drugs, DEA as the federal agency charged with enforcing the CSA, and the Office of National Drug Control Policy, as the federal coordinator of drug control policy, do not support the use of smoked marijuana for medical purposes.

C. THE PRACTICE OF MEDICINE IS IMPACTED BY MARIJUANA AS MEDICINE BALLOT INITIATIVES.

Medicine increasingly is evidence-based but marijuana has no academic presence in medical training or scholarship.

Contrary to good medical practice, there is no requirement:

a. to issue a prescription (only a recommendation)
b. extract medical history
c. give a detailed medical exam
d. discuss long term treatment, effects or follow-up
e. provide informed consent
f. consult with other physicians
g. keep proper records that support recommending marijuana instead of safe approved alternatives
h. have a good faith relationship with a patient rather than a “marijuana mill”
i. be able to identify substance abusers or the addicted.
j. Forewarn patients on maintaining control of their product

Contrary to regulations governing pharmacies, dispensaries have:
k. no product liability
l. no product regulation
m. no chain of custody
n. no accountability
o. no pharmacists trained in drug-drug interactions of appropriate dose
measures and requirements

Summary.
Over the past 150 years the US moved rapidly away from plants as medicines to purified products, for obvious reasons: the composition of a plant is unknown, the composition of its thousands of constituents are uncontrolled and the long term effects of each of these chemicals, alone or together on body, brain, behavior are unknown. At the time these ballots passed and presently, marijuana’s scientific record was not sufficient to fulfill FDA’s rigorous standards of safety, efficacy, consistent dosing and side effect profile. The evidence for smoked marijuana as a safe and effective treatment for over 12 diseases (e.g. glaucoma, Alzheimer’s disease), including the myriad forms of chronic pain that respond to different class of drugs does not begin to meet professional and FDA standards.
D. RESTRICTIVE MARIJUANA LAWS ARE DRIVEN PRIMARILY BY PERSONAL AND PUBLIC CONSIDERATIONS.

Maintaining restrictions on marijuana are more compelling than ever, as marijuana potency and availability soar, in parallel with escalating scientific evidence of marijuana’s adverse consequences.

Acute effects of marijuana on brain function.
Unlike opioids, marijuana is not likely to cause death by overdose but it resides in Schedule I because of its high abuse liability, and no medical indications – essentially because it adversely disturbs brain function and biology. A Saturday night marijuana binge is intoxicating in the short term, but it can also produce residual cognitive deficits (on learning and memory) for several days. (Marijuana 
research protocols generally wait at least 5-30 days for marijuana to clear, before measuring long term residual cognitive effects). These deficits are readily quantified, are exaggerated in schizophrenics, and refute advocacy for marijuana treatment of Alzheimer’s disease. Who is compromised by marijuana? The student in class who can’t focus, the construction worker at risk for injury, the unemployed who is less likely to find work, the poor, the high school drop-out, the criminal. It is unacceptable for soldiers, airline pilots, nuclear power plant operators, federal workers to test positive for marijuana.
Should it be acceptable for teachers, day care providers, construction workers, students, machine operators, miners, parents, or drivers? A 2009 National Highway Traffic Safety Administration (NHTSA) report showed that more people are driving on weekend nights under the influence of marijuana (8.3%) than alcohol (2.2%). Emergency department mentions of marijuana in the US have increased from 281,619 to 374,435 during 2004-2008, in parallel with linear increases in marijuana potency and marijuana addiction.

Enduring effects: marijuana addiction.
Marijuana is addictive in about 9-10% of users and progression to addiction reportedly is more rapid than progression to nicotine addiction. Abstinence in the heavily addicted unmasks physical and psychological neuroadaptation, manifest by an unnerving withdrawal syndrome. Nation-wide, more 
people harbor a medical (DSM-IV) diagnosis of marijuana abuse/addiction than any other illicit drug and more youth are DSM-IV positive for marijuana than for alcohol, as a percentage of users. Extrapolating from national statistics, an average cost for addiction treatment is $4,000 for ambulatory care and at least four times that amount for residential care. This can add billions of dollars for marijuana treatment needs nationally.
Marijuana and youth.
There is no reasonable evidence that marijuana sold for “medical purposes” will prevent diversion to young adolescents. Our abysmal failure at preventing youth cigarette smoking or alcohol consumption should be our intuitive guide. Youthful users of marijuana are at particular risk. The addiction rates of marijuana are 6-fold higher in young adolescents who initiate marijuana use at age 14 or younger. Early onset of marijuana use is also associated with addiction to other drugs in adulthood, including alcohol and heroin. Some have speculated that genetics, cigarettes smoking, social environment, poverty, child abuse, psychiatric conditions confer this higher risk in the young. But how to explain that adolescent rats exposed to the most active constituent of marijuana, delta-9-tetrahydrocannabinol or THC, only during adolescence, seek heroin at higher rates after they mature into adults compared with matched controls, and display a fundamental change in brain opioid systems long after their last dose? Social, environmental, poverty, child abuse, psychiatric conditions do not apply to inbred rats – the drug alone alters the trajectory of brain and behavioral development.

Marijuana use and neuropsychiatric disorders.
In nine population studies of more than 75,000 people from seven different countries, early marijuana use was found to be associated with an average two-fold higher risk for later-onset psychosis and schizophrenia. The influential medical journal Lancet, which declared in 1995 that “The smoking of cannabis, even long term, is not harmful to health.” changed this conclusion in 2007, by stating that “Research published since 1995, including the systematic review in 
this issue, leads us now to conclude that cannabis use could increase the risk of psychotic illness… governments would do well to invest in sustained and effective education campaigns on the risks to health of taking cannabis.” A current debate is being waged on whether to revise comparative risk assessment in the Global Burden of Disease (GBD) to include the attribution of psychosis to marijuana use. Degenhardt et al argue that the risk assessment should be included because the evidence is as good as that for many other risk
factors in the GBD. Some scientists have estimated that marijuana contributes about 8% to new cases of schizophrenia. If this estimate is accurate, unfettered marijuana access in California conceivably would add 25,000+ cases of schizophrenia, with an estimated cost of caring for this cohort for 30 years in excess of $6 billion (based on a low estimate of $8,000/per patient/year).

Long term heavy marijuana use.
Heavy daily marijuana use across protracted periods can exert harmful effects on brain tissue and mental health. Brain imaging of long-term heavy marijuana users has shown exposure-related structural abnormalities in brain regions critical for learning, memory and emotional responses, with changes associated 
with impaired verbal memory and other symptoms. Abnormal brain size and brain circuitry of adolescent marijuana users have also been recently documented. Compromised academic performance, school drop-out, and a host of other adverse consequences are elevated in high school or college students who use marijuana. Accurate price tags for these lost educational and employment opportunities don’t exist, but at the very least, they should weigh heavily on the citizens’ conscience. Peripheral health is also affected, as marijuana use is associated with increased risks for bronchitis, compromised pulmonary function, precancerous lung changes, cardiovascular events, problematic pregnancies, teratogenic and hormonal effects. Despite this evidence, 2009 was a banner year for marijuana use in our nation. Compared with 2008, 1.5 million more marijuana users were added to the ranks in 2009. The steady decline in marijuana use among youth over the past 6 years was reversed in 2009.
Marijuana use among 12-17 year olds increased by over 7%, with a 14% increase among boys, and a 13% increase among college students. Expanding acceptance of medical marijuana and proliferating availability conceivably are driving reduced perception of harm and a pivotal rise in use.

Authors’ Biography: Bertha K. Madras is a Professor of Psychobiology in the Department of Psychiatry at Harvard Medical School and former Deputy Director for Demand Reduction in the White House Office of National Drug Control Policy.

Source: Sent to Drugwatch International Feb.2 2011

Filed under: Medicine and Marijuana :

There has been much debate about whether cannabis might cause or exacerbate psychotic illnesses or whether characteristics of persons who tend to develop these conditions make them more likely to use the drug.

Authors of a new meta-analysis that found that earlier use of cannabis may trigger earlier onset of psychotic disorders say that their study supports a causative role.

Source: JAMA, March 2, 2011 – Vol. 305, No. 9

Abstract

Objective To examine the association between smoking and risk of invasive breast cancer using quantitative measures of lifetime passive and active smoking exposure among postmenopausal women.

Design Prospective cohort study. Setting 40 clinical centres in the United States. Participants 79?990 women aged 50–79 enrolled in the Women’s Health Initiative Observational Study during 1993–8. Main outcome measures Self reported active and passive smoking, pathologically confirmed invasive breast cancer.

Results In total, 3520 incident cases of invasive breast cancer were identified during an average of 10.3 years of follow-up. Compared with women who had never smoked, breast cancer risk was elevated by 9% among former smokers (hazard ratio 1.09 (95% CI 1.02 to 1.17)) and by 16% among current smokers (hazard ratio 1.16 (1.00 to 1.34)). Significantly higher breast cancer risk was observed in active smokers with high intensity and duration of smoking, as well as with initiation of smoking in the teenage years. The highest breast cancer risk was found among women who had smoked for =50 years or more (hazard ratio 1.35 (1.03 to1.77) compared with all lifetime non-smokers, hazard ratio 1.45 (1.06 to 1.98) compared with lifetime non-smokers with no exposure to passive smoking). An increased risk of breast cancer persisted for up to 20 years after smoking cessation. Among women who had never smoked, after adjustment for potential confounders, those with the most extensive exposure to passive smoking (=10 years’ exposure in childhood, =20 years’ exposure as an adult at home, and =10 years’ exposure as an adult at work) had a 32% excess risk of breast cancer compared with those who had never been exposed to passive smoking (hazard ratio 1.32 (1.04 to 1.67)). However, there was no significant association in the other groups with lower exposure and no clear dose response to cumulative passive smoking exposure.

Conclusions Active smoking was associated with an increase in breast cancer risk among postmenopausal women. There was also a suggestion of an association between passive smoking and increased risk of breast cancer.

Source: BMJ 2011; 342:d1016

Opioid use just before conception or in early pregnancy has been associated with an increased risk for birth defects, including hypoplastic left heart syndrome, one of the most critical heart defects.
According to an ongoing, population-based study conducted by the Centers for Disease Control and Prevention (CDC), women receiving opioid analgesic treatment in early pregnancy had a 2- to 3-fold increased risk of delivering infants with conoventricular septal defects, atrioventricular septal defects, hypoplastic left heart syndrome, spina bifida, or gastroschisis.
“It’s important to acknowledge that although there is an increased risk for some types of major birth defects from an exposure to opioid analgesics, that absolute risk for any individual woman is relatively modest,” principal investigator Cheryl S. Broussard, PhD, from the CDC’s National Center on Birth Defects and Developmental Disabilities, said in a news release.
“However, with very serious and life-threatening birth defects like hypoplastic left heart syndrome, the prevention of even a small number of cases is very important,” she said.

Source: The study was published online February 24 in the American Journal of Obstetrics and Gynecology.

• Those who started smoking the drug at college were 90 per cent more likely to have psychotic symptoms in their mid-20s
• Some users suffered psychotic symptoms including hallucinations, delusions and disordered thoughts
Young people who use cannabis are doubling their risk of developing psychotic symptoms, experts warn. And mental health problems persist among those who continue using it compared with those who stop, according to research by an international team of scientists.
Their study adds to mounting evidence that smoking cannabis can trigger psychotic illnesses such as schizophrenia in vulnerable youngsters. It appears to demolish counter-arguments that cannabis does not cause symptoms of mental illness, or that some turn to the drug as a form of self-medication to deal with them.
The research also shows a link with psychosis at a very early stage of use among young people who previously never experienced such symptoms. They include paranoid ideas, hallucinations, hearing voices or bizarre behaviour.
The study, by a team from Germany, the Netherlands and the Institute of Psychiatry in London, focused on more than 1,900 volunteers aged 14 to 24 living in Germany. It followed up with the group after three years and eight years.
Those who had not previously used cannabis but began to during the study had double the risk of developing psychotic symptoms, it found. If they carried on using it, they were at an increased risk of psychotic experiences compared with those who did not. There was also no evidence that suffering psychotic symptoms was likely to result in people turning to cannabis for relief.
Reporting on their findings in the British Medical Journal, the team concluded: ‘Cannabis use precedes the onset of psychotic symptoms in individuals with no history of them.’
Cannabis may also increase the risk of lasting harm to mental health by making such symptoms persist with continued use. Last month, Australian researchers found that cannabis use accelerates the onset of full-blown mental illness almost three years earlier in people at risk.
Sir Robin Murray, professor of psychiatric research at the Institute of Psychiatry, said of the latest study: ‘It is one of ten prospective studies all pointing in this same direction. In short, it adds a further brick to the wall of evidence showing that use of traditional cannabis is a contributory cause of psychoses like schizophrenia.
‘It adds new information by showing that it is those who show psychotic symptoms within a few years of initiating cannabis use who are especially likely to develop persistent psychotic symptoms if they persist in their use of cannabis.’
Previous research has shown that a quarter of the population has a genetic predisposition which makes them ten times more likely to develop psychosis and other schizophrenia-like symptoms after smoking cannabis. Experts warn that anyone with pre-existing mental health problems or family history is at increased risk of mental illness if they use cannabis.
In a BMJ commentary, Professor Wayne Hall, from the University of Queensland, and Professor Louisa Degenhardt, from the Burnet Institute in Melbourne, say the link is biologically plausible and more information should be given to young people about the risks. ‘The case is strengthened by evidence that regular cannabis use in adolescence predicts poorer educational outcomes, increased risk of using other illicit drugs, increased risk of depression and poorer social relationships in early adulthood’, they added.

Source: http://www.dailymail.co.uk/health/article 2nd March 2011

Although growing literature suggests that long-term marijuana use is associated with a wide range of adverse health consequences, many people believe it is relatively harmless and should be legalized, the researchers noted. “However, this study shows long-term, heavy cannabis use causes significant brain injury, memory loss, difficulties learning new information, and psychotic symptoms, such as delusions of persecution [paranoia], delusions of mind-reading, and bizarre social behaviors in even non-vulnerable users,” said lead researcher Murat Yucel, from the ORYGEN Research Centre and the Neuropsychiatry Centre at the University of Melbourne.
This new evidence plays an important role in further understanding the effects of marijuana and its impact on brain functioning, Yucel said. “The study is the first to show that long-term cannabis use can adversely affect all users, not just those in the high-risk categories such as the young, or those susceptible to mental illness, as previously thought,” he said.
The report was published in the June issue of the Archives of General Psychiatry.
In the study, Yucel’s team did high-resolution MRIs on 15 men who smoked more than five joints a day for more than 10 years. They compared those with scans of 16 men who did not In addition, all the men took verbal memory tests and were examined for symptoms of psychiatric disorders. “The more marijuana used, the more these individuals were likely to show reduced brain volumes in the hippocampus and amygdala, as well as being more likely to develop symptoms of psychotic disorders and to have significant memory impairment,” Yucel said.
In fact, the hippocampus of marijuana users was 12 percent smaller, and the amygdala was 7.1 percent smaller than among nonusers. In addition, men who used marijuana also had symptoms of psychiatric disorders, Yucel’s group found. The hippocampus is associated with the regulation of emotion and memory, while the amygdala controls fear and aggression.
“There is ongoing controversy concerning the long-term effects of cannabis on the brain,” Yucel said. “These findings challenge the widespread perception of cannabis as having limited or no harmful effects on brain and behavior. Although modest use may not lead to significant neurotoxic effects, these results suggest that heavy daily use might indeed be toxic

SOURCE: Murat Yucel, Ph.D., ORYGEN Research Centre, Melbourne Neuropsychiatry Centre, University of Melbourne, Australia; Adam Bisaga, M.D., assistant professor, psychiatry, Columbia University, and addiction psychiatrist, New York State Psychiatric Institute, New York City; June 2008, Archives of General Psychiatry

Abstract

The nature of addiction is often debated along moral versus biological lines. However, recent advances in neuroscience offer insights that might help bridge the gap between these opposing views. Current evidence shows that most drugs of abuse exert their initial reinforcing effects by inducing dopamine surges in limbic regions, affecting other neurotransmitter systems and leading to characteristic plastic adaptations. Importantly, there seem to be intimate relationships between the circuits disrupted by abused drugs and those that underlie self-control. Significant changes can be detected in circuits implicated in reward, motivation and/or drive, salience attribution, inhibitory control and memory consolidation. Therefore, addiction treatments should attempt to reduce the rewarding properties of drugs while enhancing those of alternative reinforcers, inhibit conditioned memories and strengthen cognitive control. We posit that the time has come to recognize that the process of addiction erodes the same neural scaffolds that enable self-control and appropriate decision making.

Source: Trends in Molecular Medicine, Volume 12, Issue 12, 559-566, 1 December 2006

Summary

Addiction coopts the brain’s neuronal circuits necessary for insight, reward, motivation, and social behaviors. This functional overlap results in addicted individuals making poor choices despite awareness of the negative consequences; it explains why previously rewarding life situations and the threat of judicial punishment cannot stop drug taking and why a medical rather than a criminal approach is more effective in curtailing addiction.

Source: Neuron, Volume 69, Issue 4, 599-602, 24 February 2011

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 effect, 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 effect was present for both psychotic and affective outcomes.

Interpretation

The evidence is consistent with the view that cannabis increases risk of psychotic outcomes independently of confounding and transient intoxication effects, although evidence for affective 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 sufficient evidence to warn young people that using cannabis could increase their risk of developing a psychotic illness later in life.

Source: The Lancet, Volume 370, Issue 9584, Pages 319 – 328, 28 July 2007

Some 56 heroin-dependent patients who had undergone detoxification treatment and were particularly motivated to remain heroin-free took part in a research study. Half of the participants were implanted with a total of 20 subcutaneous pellets containing naltrexone, which was gradually released from a saline solution with the aim of producing a six-month blockage effect. All the participants continued their normal follow-up treatments while the study was ongoing.
After six months, over twice as many in the group receiving naltrexone as in the control group (11 out of 23 as opposed to 5 out of 26) managed to refrain from using heroin and other morphine substances. Heroin use among those patients receiving naltrexone who did not manage to discontinue using heroin altogether was more than halved compared with their level of heroin use before they started treatment. In the control group the majority of patients relapsed to daily heroin use.
Satisfaction with the naltrexone implants was high. On a scale from 0 to 100 the participants gave the capsules a score of 85.

Clear-cut findings

Helge Waal, Professor emeritus at SERAF, would like to see the naltrexone implant included as one of the treatment options offered to heroin-dependent patients in Norway.
“Although this is a relatively small-scale study, the findings are so clear-cut that we think this should become an important treatment option for substance abusers.”

Source: The Research Council of Norway (2011, February 17) Retrieved February 18, 2011, from http://www.sciencedaily.com

Contact address: Fabrizio Faggiano, Department of Medical Sciences, University of Piemonte Orientale A. Avogadro, Via Santena 5 bis, Novara, 28100, Italy. fabrizio.faggiano@med.unipmn.it.
Editorial group: Cochrane Drugs and Alcohol Group.
Publication status and date: Edited (no change to conclusions), published in Issue 3, 2008.

Citation: Faggiano F, Vigna-Taglianti F, Versino E, Zambon A, Borraccino A, Lemma P. School-based prevention for illicit drugs’ use. Cochrane Database of Systematic Reviews 2005, Issue 2. Art. No.: CD003020. DOI: 10.1002/14651858.CD003020.pub2.

Copyright © 2008 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.
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Abstract

Background

Drug addiction is a chronic, relapsing disease. Primary interventions should be aimed to reduce first use, or prevent the transition from experimental use to addiction. School is the appropriate setting for preventive interventions.
Objectives
To evaluate the effectiveness of school-based interventions in improving knowledge, developing skills, promoting change, and preventing or reducing drug use versus usual curricular activities or a different school-based intervention .
Search strategy
We searched the Cochrane Drug and Alcohol Group trial register (February 2004), the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 2, 2004), MEDLINE (1966 to February 2004) , EMBASE (1988 to February 2004), and other databases. We also contacted researchers in the field and checked reference lists of articles.
Selection criteria
Randomised controlled trials (RCT), case controlled trials (CCT) or controlled prospective studies (CPS) evaluating school-based interventions designed to prevent substance use.
Data collection and analysis
Two authors independently extracted data and assessed trial quality.
Main results
32 studies (29 RCTs and three CPSs) were included with 46539 participants. Twenty eight were conducted in the USA; most were focused on 6th-7th grade students, and based on post-test assessment.

RCTs

(1) Knowledge versus usual curricula
Knowledge focused programs improve drug knowledge (standardised mean difference (SMD) 0.91; 95% confidence interval (CI) 0.42 to 1.39).
(2) Skills versus usual curricula
Skills based interventions increase drug knowledge (weighted mean difference (WMD) 2.60; 95% CI 1.17 to 4.03), decision making skills (SMD 0.78; CI 95%: 0.46 to 1.09), self-esteem (SMD 0.22; CI 95% 0.03 to 0.40), peer pressure resistance (relative risk (RR) 2.05; CI 95%: 1.24 to 3.42), drug use (RR 0.81; CI 95% 0.64 to 1.02), marijuana use (RR 0.82; CI 95% 0.73 to 0.92) and hard drug use (RR 0.45; CI 95% 0.24 to 0.85).
(3) Skills versus knowledge
No differences are evident.
(4) Skills versus affective
Skills-based interventions are only better than affective ones in self-efficacy (WMD 1.90; CI 95%: 0.25 to 3.55).

Results from CPSs

No statistically significant results emerge from CPSs.
Authors’ conclusions
Skills based programs appear to be effective in deterring early-stage drug use.
The replication of results with well designed, long term randomised trials, and the evaluation of single components of intervention (peer, parents, booster sessions) are the priorities for research. All new studies should control for cluster effect.
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Plain language summary

School-based prevention for illicit drugs’ use
Drug addiction is a long-term problem caused by an uncontrollable compulsion to seek drugs. People may use drugs to seek an effect, to feel accepted by their peers or as a way of dealing with life’s problems. Even after undertaking detoxification to reach a drug-free state, many return to opioid use. This makes it important to reduce the number of people first using drugs and to prevent transition from experimental use to addiction. For young people, peers, family and social context are strongly implicated in early drug use. Schools offer the most systematic and efficient way of reaching them. School programs can be designed to provide knowledge about the effects of drugs on the body and psychological effects, as a way of building negative attitudes toward drugs; to build individual self-esteem and self-awareness, working on psychological factors that may place people at risk of use; to teach refusal and social life skills; and to encourage alternative activities to drug use, which instil control abilities.
The review authors found 32 controlled studies, of which 29 were randomised, comparing school-based programs aimed at prevention of substance use with the usual curriculum. The 46,539 students involved were mainly in sixth or seventh grade. Programs that focused on knowledge improved drug knowledge to some degree, in six randomised trials. Social skills programs were more widely used (25 randomised trials) and effectively increased drug knowledge, decision-making skills, self-esteem, resistance to peer pressure, and drug use including of marijuana (RR 0.8) and hard drugs (heroin) (RR 0.5). The programs were mainly interactive and involved external educators in 20 randomised trials. Effects of the interventions on assertiveness, attitudes towards drugs, and intention to use drugs were not clearly different in any of the trials.
Most trials were conducted in the USA and, as a nation’s social context and drug policies have a significant influence on the effectiveness of the programs, these results may not be relevant to other countries. Measures of change were often made immediately after the intervention with very little long-term follow up or investigation of peer influence, social context, and involvement of parents.

Source: http://onlinelibrary.wiley.com and www.cochranlibrary.com 2008

Two of the most widely recommended US school and family prevention programmes retarded growth in some forms of substance use, especially among youngsters who had already used by their early teens, but there are some methodological concerns over the findings.
Summary 36 secondary schools in the rural US mid-west were randomly allocated to either carry on as normal (the control schools) or to one of two prevention programmes. Both were delivered primarily in the seventh grade (ages 12–13), and both featured the LifeSkills Training (LST) drug education curriculum consisting of fifteen classroom lessons with later ‘boosters’. In one set of schools, these lessons were supplemented by the Strengthening Families Program: for Parents and Youth 10-14. This entails seven two-hour evening sessions plus four booster sessions in the following year, during which groups of about six or seven families focus in turn on particular parenting issues and skills. In the first hour of each session, parents and children learn in parallel; in the second, they come together to practice these skills with each other. Only a quarter of the families allocated to these (and 38% of those actively recruited) attended any of the family sessions, but results are reported for all the families offered the intervention, regardless of attendance.
Questionnaire responses from 1677 pupils surveyed about six months before the grade seven lessons formed the baseline to assess changes in substance use among the same pupils over each of the five years following the lessons. Typically by then aged 17–18, about three quarters of the starting sample responded to the final assessments. For the featured report the sample was narrowed down slightly to pupils who had provided the relevant outcome measures at least three times: at baseline; about a month after the seventh grade interventions; and during at least one follow-up. For these pupils, the analysis tested whether over the five and a half years:
• trends in the growth of substance use differed between the three sets of schools; and
• whether by the end levels of substance use also differed.
First the study assessed how many pupils had started to use alcohol, cigarettes or cannabis. Most consistently positive results were found for cigarettes; growth in the proportion who had tried smoking, and the final proportion who had used by age 17–18, were significantly lower in intervention schools compared to control schools. For cannabis, only the final proportion was significantly lower, and for alcohol, only the growth trend, and then only when the family intervention had supplemented the lessons. When these measures were combined in an index representing experience of all three substances, both the growth trend and the final outcomes favoured the interventions. Experience of getting drunk was also measured and, like drinking itself, only the growth trend favoured the interventions.
Similar analyses for current use on at least a monthly basis and other more serious patterns of substance use found no results favouring the interventions. However, there were such results among the fifth of pupils considered at high risk of developing substance use problems. These were the pupils who at the first survey point at age 12–13 had already used two of the three substances. Compared to their lower risk peers, among these pupils both interventions had consistently greater effects on overall levels of use across the follow-up years. Further analysis showed that among lower risk pupils, the interventions made no significant difference. But among the higher risk fifth, growth in the average frequency of smoking cigarettes or using cannabis was less than in the control schools, and so too was final average frequency of use. This was not the case for the frequency of drinking or of getting drunk; for these measures only two of the eight outcomes significantly favoured the interventions. Among the same higher risk pupils, indices of serious use patterns combining measures of current or past use of all three substances consistently favoured the intervention schools.
Summarising their findings, the authors noted that for all substance initiation outcomes, one or both intervention groups showed significant, positive differences compared with the control group in the final follow-up year, and/or significant differences in growth trends over the five years since the interventions. In contrast, across all the pupils, more serious substance use outcomes reflecting mainly current and frequent use were not significantly affected. However, these forms of substance use were curbed when the analysis was restricted to higher risk pupils. Though the two interventions often bettered education-as-usual, in no case did one outperform the other. The authors speculated that less convincing initiation-prevention results than in earlier studies might have been due to the family intervention being delayed a year, when more pupils had already initiated substance use. In terms of affecting more serious forms of substance use, pupils already advanced in their substance use patterns responded relatively well, possibly because the messages were more ‘real’ for them and for their parents. Despite randomisation, there remained some significant baseline differences between control and intervention pupils which might also have obscured intervention impacts, though attempts were made to adjust for these in the analyses.
The two programmes tested in the study enjoy among the most widely respected research records in substance use prevention (LST SFP). The featured study’s strengths include large samples, reasonable follow-up rates, randomisation by school and an analysis controlling for the influence of the school itself, and outcome measures probing not just experience of the substances concerned, but how serious and lasting this was. Nevertheless the most which can be said is that the LifeSkills Training element probably retarded the initiation of smoking, possibly cannabis use, but not drinking, had no cross-sample benefits in respect of the forms of substance use of greatest concern, but may have had such benefits among the minority of pupils already relatively advanced in their substance use before the interventions started. Other LifeSkills Training studies have also most consistently found beneficial outcomes in respect of smoking, the programme’s original target.
Focusing on the featured study’s positive findings might give the impression of more all round success, but in respect of the full samples, these consisted of at most 13 out of 44 findings, and possibly (if arguably more appropriate methodological conventions had been followed) seven or fewer. Greater and more consistent success among the higher risk pupils is a tentative finding because of differences between intervention and control schools, because the study was not set up to test this subsample, and because of some methodological issues. Impacts on the forms of drug use of greatest concern emerged solely from this analysis, meaning that the interventions’ ability to reduce these cannot be considered to have been demonstrated, though the possibility that this might prove to be the case is encouraging. Importantly, though many tests did not show the interventions were superior to education-as-usual, none indicated that they were inferior; the only significant findings favoured the interventions. For more on all these issues see background notes.
Disappointingly, and despite earlier findings from the study, there was no real hint that adding the family programme improved on the school lessons in terms of the substance use measures reported in the study, though there may have been other benefits. Remaining support for the family programme comes mainly from a study whose findings (impressive as they were) derived from just over a third of the mainly white and rural families asked to participate in the study. A similar limitation applies to a later study of a substantially revised version among poor black families. Because of the way they were designed, these trials could establish benefits only among the minority of families prepared or able to participate in the interventions and complete the studies; they cannot be considered a secure indication of how the interventions would perform if applied across the board. So far in the UK a small pilot study has established the programme’s feasibility among a small set of families.
This leaves two of the most thoroughly researched universal prevention programmes for children of secondary school age with mixed findings of uncertain relevance to how they might perform if truly applied across the board. At least part of the problem lies in not in whether the benefits of these programmes are (or at least, can be) real, but in the difficulty of showing they are real. Verdicts in respect of drinking that public health strategies built on education and persuasion are relatively ineffective compared to measures such as restricting availability and raising price, would not be altered by the featured study. For smoking, the case for education in schools as a public health strategy is considerably stronger. Universal prevention programmes in general, and school-based programmes in particular, have greater impacts on tobacco use than on use of the other two substances featured in the study.
Some evidence supports the modest effectiveness of school programmes in preventing cannabis use. But of the four studies on which this verdict was based, one was a primary school programme not focused on substance use at all but on classroom management, education and parenting, another was conducted only among pupils for some reason excluded from mainstream education, and the programme studied in a third has since failed in a more real-world study conducted by researchers not associated with its development. The remaining study was conducted in secondary schools and concerned LifeSkills Training, but the impact on cannabis use was not statistically significant. This line up does not offer much support to drug education in mainstream secondary schools as a means of preventing cannabis use.
Mixed findings of a prevention impact from school programmes targeting substance use do not negate the possibility that general attempts to create schools conducive to healthy development will affect substance use along with other behaviours, nor do they relieve schools of the obligation to educate their pupils on this important aspect of our society. As much as the limited research, such considerations led the UK’s National Institute for Health and Clinical Excellence (NICE) to recommend that alcohol education should be an integral part of national science and health education curricula, in line with government guidance.
Thanks for their comments on this entry in draft to Richard Spoth of Iowa State University, Andrew Brown of the Drug Education Forum and David Foxcroft of Oxford Brookes University. Commentators bear no responsibility for the text including the interpretations and any remaining errors.
Last revised 02 July 2009

Source: Spoth R.L., Randall G.K., Trudeau L. et al.
Drug and Alcohol Dependence: 2008, 96(1–2), p, 57–68.

Just under 9% of HIV-positive individuals in the UK are co-infected with hepatitis C virus, investigators report in the Journal of Viral Hepatitis.
“In comparison with other large cohort studies, the overall HCV [hepatitis C virus] prevalence of 8.9% in the UK…is low,” comment the investigators. They believe that this is because of the low prevalence of HIV among injecting drug users in the UK. However, approximately 20% of HIV-positive patients in the UK have never been tested for hepatitis C, despite guidance that all patients should be screened annually.
Encouragingly, there was no evidence that co-infection resulted in a poorer response to antiretroviral therapy. Liver disease caused by hepatitis C is now a major cause of illness and death in HIV-positive patients. However, detailed information on the prevalence of hepatitis C among HIV-positive individuals in the UK is lacking. There is also little information on hepatitis C testing and the impact of co-infection on responses to HIV therapy
Therefore investigators from the UK Collaborative HIV Cohort (UK CHIC) undertook an observational study involving 31,765 patients provided with care at ten specialist HIV clinics between 1996 and 2007. Prevalence of co-infection (determined by a positive hepatitis C antibody result), trends in testing, and responses to HIV therapy were monitored. Overall, 64% of patients had been tested for hepatitis C at least once. The proportion of patients screened for the virus increased from 9% in 1996 to 80% in 2007.
“There has been a clear instruction that all HIV-positive patients should be screened since at least 2004,” write the investigators. Nevertheless, “20% of patients under follow-up in 2007 had not apparently ever been tested. The latest BHIVA [British HIV Association] guidelines recommend screening all HIV-positive patients at diagnosis, with annual repeat testing in those who are negative.”
Testing rates differed according to HIV risk group, and was highest for gay men (74%), followed by heterosexual men and women (63%). Although injecting drug use is a well-established risk factor for hepatitis C, only 50% of individuals with a history of injecting drug use had been tested for the virus.
However, the investigators think that the true prevalence of testing in this group is likely to be higher. They comment: “these patients may be more likely to have been tested previously.” The researchers also suggest that the higher rates of mortality and loss to follow-up among injecting drug users could also mean this group were less likely to be screened for hepatitis C.
Overall prevalence of hepatitis C was 9%, and prevalence was 8% among those who were receiving care in 2007. By contrast, prevalence in the general UK population is estimated to be 0.44%. The investigators suggest that the significantly higher prevalence of the infection among patients in the UK CHIC reflects “the shared transmission routes of HCV and HIV.”
Prevalence of hepatitis C differed between HIV risk groups. It was highest in injecting drugs users (84%), followed by gay men (7%), and heterosexual men and women. However, the investigators suggest that some hepatitis C infections in gay men may actually be due to injecting drug use, who suggest that this behaviour may be “underreported by some MSM [men who have sex with men], sufficient to place them at risk of HCV infection…underreporting of IDU as a risk for HCV transmission in MSM may also affect other cohorts.”
Most co-infected patients were men (80%), white (82%), and their median age was 37. The strongest independent risk factor for co-infection with hepatitis C was HIV transmission group. Injecting drug users were significantly more likely to be co-infected than all other risk groups (p < 0.0001). The impact of co-infection on responses to antiretroviral therapy was analysed in the 9669 patients who started HIV treatment after 2000. A total of 4% of these patients were co-infected. Overall, 91% of patients achieved an undetectable viral load. Co-infected patients were just as likely as individuals who were only infected with HIV to achieve this outcome. There was no association between co-infection and subsequent rebound in viral load. In addition, CD4 cell count increases were comparable between co-infected and HIV-mono-infected patients. “We found no association between HCV co-infection and either the initial virological response, the rate of viral rebound or the CD4 count response,” emphasise the investigators. They note that results from the Swiss HIV cohort study showed that co-infection did not have an impact on virological responses to therapy. “The overall cumulative prevalence of HCV of 8.9% in UK CHIC is lower than other cohorts among whom the proportion of IDU is higher,” conclude the researchers. However, they emphasise that this rate of co-infection still “represents a substantial burden of disease.” Source:www.aidsmap.com Feb 14th 2011

Young people who misuse drugs and alcohol are at a greater risk for continuing this behavior into their middle-aged years, according to research by Yasmina Molero Samuelson at Sweden’s Center for Psychiatric Research (CPF), Karolinska Institutet. They are also more likely to suffer from physical, financial and mental health problems and experience more accidents, suicide attempts and premature death.
“What we can see is that adolescent antisocial behavior, manifested through substance misuse and delinquency, significantly increases the risk of various types of psychosocial problems in adulthood, even into middle age,” said Samuelson.
Samuelson analyzed two large groups of adolescents who had been in treatment for drug use at a clinic in Stockholm, Sweden during the end of the 1960s and the beginning of the 1980s. The analysis ended in 2002, and the participants were compared to two matched samples from the average population.
The results revealed that teens treated for substance abuse continued to suffer from psychosocial problems well after treatment, even up to age 50, to a far greater extent than those in the matched samples. They also had a higher risk of experiencing several coexisting problems in adulthood.
Interestingly, females with substance abuse issues and delinquency showed an equal risk of developing psychosocial problems as adults as their male counterparts. A significant number of girls who were treated at the clinic committed crimes in both adolescence and adulthood. Overall, the crimes committed by both males and females included non-violent crimes, violent crimes, and substance-related crimes.
“This emphasizes the importance of early and effective interventions in order to prevent a negative development that risks being maintained for most of a person’s life,” said Samuelson.
The variety of problems still experienced well into adulthood suggests that treatment interventions during teen years should not only focus on the specific substance abuse or delinquency, but should also evaluate and treat problems in other areas of life as well.
“The results also clearly show the importance of not overlooking young girls in these types of contexts, since they too demonstrate severe antisocial behavior, and are equally at risk of developing problems throughout their lives as their male counterparts,” said Samuelson.

Source: www.psychcentral.com 11 Feb.2011

Abstract:

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.
(Full text available here) – http://archpsyc.ama assn.org/cgi/content/full/archgenpsychiatry.2011.5

Source: . Archives of General Psychiatry, 7th February 2011

Research Summary

Researchers say that a drug that blocks a brain protein called NK1R (neurokinin-1 receptor) involved in stress response appears to reduce alcohol craving, ABC News reported Feb. 14.
Building on studies showing that mice lacking NK1R seemed to lose interest in alcohol, researchers from the National Institute on Alcohol Abuse and Alcoholism gave NK1R-blocking drugs to a group of 25 alcoholics and compared their craving responses to those of 25 other alcoholics given a placebo. Those receiving the blocking drug reported about half the level of craving for alcohol as the control group.
Markus Heilig, NIAAA’s clinical director, said the study points to a new approach to addiction treatment by focusing on reducing craving rather than preventing the pleasurable effects of alcohol consumption. “We’re really trying to open up a new category of treatments that would help most people,” he said.
“This is a potentially important finding which indicates a novel mechanism for reducing craving in individuals who drink to reduce high anxiety,” said pharmacology expert Boris Tabakoff of the University of Colorado at Denver.
“It may be that this medication would help alcoholics who drink when stressed,” added Charles O’Brien of the Treatment Research Center for the University of Pennsylvania Health System, although he stressed: “It is wrong to think of all alcoholics as alike.”
The study was published online in the journal Science.

Source: Join Together Feb. 2008

Research Summary
People in recovery from alcohol addictions can suffer sleep disruptions for months or years after they stop drinking,
Researchers at SRI International monitored the brain activity during sleep of a group of 42 people in recovery and compared the results to brain scans of nondrinkers. They found that men and women in recovery spent significantly less time in light, stage-one sleep and slow-wave sleep — the latter essential for memory — and somewhat more time in REM sleep, when dreaming normally occurs.
Researcher Ian Colrain and colleagues said the sleep disruptions probably worsen the mental problems associated with long-term drinking.

Source: Sleep. Oct. 1, 2009

Why do otherwise good kids seem to make bad decisions when they are with their friends? New research on risk taking and the teenage brain offers some answers.
In studies at Temple University, psychologists used functional magnetic resonance imaging scans on 40 teenagers and adults to determine if there are differences in brain activity when adolescents are alone versus with their friends. The findings suggest that teenage peer pressure has a distinct effect on brain signals involving risk and reward, helping to explain why young people are more likely to misbehave and take risks when their friends are watching.
To test how the presence of peers influences risk taking, the researchers asked 14 young teenagers (ages 14 to 18), 14 college students and 12 young adults to play a six-minute video driving game while in a brain scanner. Participants were given cash prizes for completing the game in a certain time, but players had to make decisions about stopping at yellow lights, and being delayed, or racing through yellow lights, which could result in a faster time and a bigger prize, but also meant a higher risk for crashing and an even longer delay. The children and adults played four rounds of the game while undergoing the brain scan. Half the time they played alone, and half the time they were told that two same-sex friends who had accompanied them to the study were watching the play in the next room.
Among adults and college students, there were no meaningful differences in risk taking, regardless of whether friends were watching. But the young teenagers ran about 40 percent more yellow lights and had 60 percent more crashes when they knew their friends were watching. And notably, the regions of the brain associated with reward showed greater activity when they were playing in view of their friends. It was as if the presence of friends, even in the next room, prompted the brain’s reward system to drown out any warning signals about risk, tipping the balance toward the reward.
“The presence of peers activated the reward circuitry in the brain of adolescents that it didn’t do in the case of adults,” said Laurence Steinberg, an author of the study, who is a psychology professor at Temple and author of “You and Your Adolescent: The Essential Guide for Ages 10 to 25.” “We think we’ve uncovered one very plausible explanation for why adolescents do a lot of stupid things with their friends that they wouldn’t do when they are by themselves.”
Dr. Steinberg notes that the findings give a new view of peer pressure, since the peers in this experiment were not even in the same room as the teenager in the scanner.
“The subject was in the scanner, so the friends were not able to directly pressure the person to take chances,” Dr. Steinberg said. “I think it’s helpful to understand because many parents conceive of peer pressure as kids directly coercing each other into doing things. We’ve shown that just the knowledge that your friends are watching you can increase risky behavior.”
Dr. Steinberg notes that the brain system involved in reward processing is also involved in the processing of social information, explaining why peers can have such a pronounced effect on decision making. The effect is believed to be especially strong in teenagers because brain changes shortly after puberty appear to make young people more attentive and aware of what other people are thinking about them, Dr. Steinberg said.
The study results are borne out in real-world data that show teenagers have a much higher risk of car accidents when other teenagers are in the car. More study is needed to determine if the effect shown in the game study is the same when teenagers are in the presence of an opposite-sex friend or romantic interest. In the study, there were no meaningful differences in risk taking among boys and girls. However, some real-world driving data suggests that teenage boys take more risks behind the wheel when one or more boys are in the car, but drive more carefully if they are with a girlfriend.
For parents, the study data reinforce the notion that groups of teenagers need close supervision.
“All of us who have very good kids know they’ve done really dumb things when they’ve been with their friends,” Dr. Steinberg said. “The lesson is that if you have a kid whom you think of as very mature and able to exercise good judgment, based on your observations when he or she is alone or with you, that doesn’t necessarily generalize to how he or she will behave in a group of friends without adults around. Parents should be aware of that.”

Source: New York Times 5 Feb 2011

Filed under: Brain and Behaviour,Youth :

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