Prevention of Youthful Marijuana Use.

Considerable money and effort have been expended in attempts to prevent drug use by youth, with disappointing results. Too often, prevention programs have singled out youth with simplistic messages of exaggerated risk and the same politically acceptable solution for all-abstinence. Historically, prevention efforts have been less effective by not being soundly based in science and failing also to address adult drug and alcohol use as part of the problem. The Institute of Medicine continuum of care model developed in 1994 offers a framework for a more sophisticated, three-tiered approach to prevention, defined as all services provided prior to a clinical diagnosis of a substance use disorder. By dividing prevention efforts into universal (delivered to broad populations without consideration of individual risk for developing substance use disorder), selected (targeting sub-groups of individuals identified on the basis of characteristics known to create an elevated risk for substance use disorder), and indicated (addressing individuals identified on the basis of manifest risk behaviors), prevention can be better tailored to meet different levels of need. Student Assistance Programs (SAPs) and community coalitions provide examples of how IOM's continuum of care model can be integrated into drug prevention programs for youth.

Mitigation of Marijuana-Related Legal Harms to Youth in California.

If recreational marijuana is legalized for adults in California, a rational implementation of public policy would neither criminalize youth possession, nor medically pathologize it by conflating possession with addiction. The harms of a criminal justice approach to juveniles should not exceed the harms of the drug itself. Juvenile arrests and probation have consequences: (1) arrest records, probation, and juvenile hall; (2) an incarceration subculture, "crime school," psychological and re-entry costs; (3) school "zero-tolerance" expulsions and suspensions; (4) ineligibility for federal school loans; (5) employment screening problems; (6) racial disparities in arrests; (7) fines and attorney's fees; and (8) immigration/naturalization problems. Marijuana-related arrest rates in California dropped after a 2011 law making possession under 1 oz. an infraction for all, but juvenile marijuana arrests continue to outnumber arrests for hard drugs. Recommendations for prudent implementation policy include: stable marijuana tax funding for Student Assistance Programs (SAPs) in high schools; elimination of "zero-tolerance" suspension/expulsion policies in favor of school retention and academic remediation programs; juvenile justice transparency discriminating among infractions, misdemeanors, and felonies. Criminal sanctions and durations must be proportional to the offense. Probation-based interventions should be reserved for larger possession amounts and recidivist offenders, and outcomes should be independently evaluated.

Intensive intervention for alcohol-dependent smokers in early recovery: a randomized trial.

INTRODUCTION: The purpose of this study was to investigate the efficacy of an intensive tobacco cessation intervention for alcohol-dependent smokers in early recovery. METHODS: A total of 162 alcohol-dependent smokers were randomized to either intensive intervention for smoking cessation or usual care. The intensive intervention consisted of 16 sessions of individual cognitive behavior therapy (CBT) and combination nicotine replacement therapy that lasted 26 weeks. Usual care involved referral to a free-standing smoking cessation program that provided smoking cessation counseling of varying duration and guideline-concordant medications. The primary cessation outcome was verified 7-day point prevalence abstinence (PPA) at 12, 26, 38, and 52 weeks. RESULTS: At 12 and 26 weeks, the verified 7-day point-prevalence quit rate was significantly higher for the intensive intervention group than for the usual care group (both p=0.03). However, the quit rates for the two treatment groups were not significantly different at 38 or 52 weeks. Verified 30-day alcohol abstinence rates were not significantly different for the two treatment groups at any of the follow-up assessments. CONCLUSIONS: The intensive smoking cessation intervention yielded a higher short-term smoking quit rate without jeopardizing sobriety. A chronic care model might facilitate maintenance of smoking cessation during the first year of alcohol treatment and perhaps for longer periods of time. It is hoped that studies such as this will inform the development of more effective interventions for concurrent alcohol and tobacco use disorders.

Chronic cigarette smoking modulates injury and short-term recovery of the medial temporal lobe in alcoholics.

Memory function is largely mediated by the medial temporal lobe (MTL), and its compromise has been observed in alcohol dependence and chronic cigarette smoking. The effects of heavy alcohol consumption and chronic smoking on hippocampal volumes and MTL metabolites and their recovery during abstinence from alcohol have not been assessed. Male alcoholics in treatment (ALC) [13 smokers (sALC) and 11 non-smokers (nsALC)] underwent quantitative magnetic resonance imaging and short-echo proton magnetic resonance spectroscopic imaging at 1 week and 1 month of sobriety. Outcome measures were compared with 14 age-matched, non-smoking light-drinkers and were related to visuospatial learning and memory. Over 1 month of abstinence, N-acetyl-aspartate, a neuronal marker, and membrane-associated choline-containing metabolites normalized in the MTL of nsALC subjects, but remained low in the MTL of sALC subjects. Metabolite concentration changes in both groups were associated with improvements in visuospatial memory. Hippocampal volumes increased in both groups during abstinence, but increasing volumes correlated with visuospatial memory improvements only in nsALC subjects. In summary, chronic cigarette smoking in alcohol-dependent men appears to have adverse effects on MTL metabolite recovery during short-term sobriety. These data may also have implications for other conditions with established MTL involvement and significant smoking co-morbidity, such as schizophrenia-spectrum and mood disorders.

Chronic smoking is associated with differential neurocognitive recovery in abstinent alcoholic patients: a preliminary investigation.

BACKGROUND: Approximately 50 to 90% of individuals in North America seeking treatment for alcoholism are chronic smokers. A growing body of evidence suggests that chronic cigarette smokers show a pattern of neurocognitive dysfunction similar to that observed in alcoholic patients. However, previous studies investigating neurocognitive recovery in abstinent alcoholic patients did not specifically consider the potential effects of chronic cigarette smoking. METHODS: This study comprehensively compared longitudinal neurocognitive changes over 6 to 9 months of abstinence among 13 nonsmoking recovering alcoholic patients (ALC) and 12 actively smoking ALC. The neurocognitive performance of the alcoholic groups was compared with nonsmoking light-drinking controls (nonsmoking LD). RESULTS: Nonsmoking ALC exhibited a significantly greater magnitude of longitudinal improvement than smoking ALC on measures of cognitive efficiency, executive skills, visuospatial skills, and working memory. Both nonsmoking ALC and smoking ALC demonstrated equivalent improvement on auditory-verbal learning, auditory-verbal memory, and processing speed. Nonsmoking LD showed no significant changes in neurocognition over time. In cross-sectional comparisons at 6 to 9 months of abstinence, nonsmoking ALC were superior to smoking ALC on measures of auditory-verbal learning, auditory-verbal memory, cognitive efficiency, executive skills, processing speed, and working memory. The longitudinal and cross-sectional neurocognitive differences observed between nonsmoking and smoking ALC remained significant after covarying for group differences in education, estimated premorbid intelligence alcohol consumption, and other potentially confounding variables. In smoking ALC, greater smoking severity was inversely related to longitudinal improvement on multiple neurocognitive measures. CONCLUSIONS: These preliminary results suggest that chronic smoking may modulate neurocognitive recovery in abstinent alcoholic patients. More generally, chronic smoking may impact neurocognition in other conditions where is it a prevalent behavior.

Addressing nicotine dependence in psychodynamic psychotherapy: perspectives from residency training.

OBJECTIVE: According to APA treatment recommendations, psychiatrists should assess and intervene in tobacco use with all of their patients who smoke. The ease with which this occurs may vary by treatment model. This study examined perspectives in residency training to identify a framework for addressing nicotine dependence within psychodynamic psychotherapy. METHOD: The authors collected data from a focus group of psychiatry residents and interviews with psychiatry residency faculty with expertise in psychodynamic psychotherapy. The transcribed interviews were analyzed for key themes and synthesized. RESULTS: Though the residents reported hesitancy to address patients' tobacco use, specifically in psychodynamic psychotherapy, the consensus from the expert faculty consultants was that tobacco interventions can and should be incorporated. The faculty provided suggestions, consistent with a psychodynamic formulation, for assessing patients' tobacco use and their interest in quitting, providing cessation treatment and/or referrals, and following up with patients to address relapse. CONCLUSIONS: The findings provide a useful framework, consistent with a psychodynamic model, for assessing and treating tobacco use with patients. Additional training and supervision likely are needed to increase residents' confidence and comfort with implementing these strategies.

A comparison of neurocognitive function in nonsmoking and chronically smoking short-term abstinent alcoholics.

Approximately 70-90% of individuals in North America seeking treatment for alcoholism are chronic smokers. A growing body of evidence suggests chronic cigarette smoking alone adversely affects neurocognition in adults. However, few studies on the neurocognitive function of short-term abstinent alcoholics have specifically considered the potential effects of chronic cigarette smoking. In this study, 20 nonsmoking recovering alcoholics (nsRA) and 22 actively smoking recovering alcoholics (sRA) participants, matched on age and education, were contrasted on a comprehensive neurocognitive battery after 34+/-9 days of abstinence. nsRA were superior to sRA on measures of auditory-verbal learning and memory, processing speed, cognitive efficiency, and static postural stability. These group differences were not a function of group disparities in age, education, estimated premorbid verbal intelligence, lifetime alcohol consumption, or other measured comorbid psychiatric or medical factors. In sRA, longer smoking duration was negatively correlated with executive skills, visuospatial learning, general cognitive efficiency, and static postural stability. These results indicate that greater consideration of the potential neurobiological effects of current chronic smoking on neurocognitive functioning is warranted in studies of alcoholism and other conditions where smoking is a common comorbid factor.

Effects of chronic alcohol dependence and chronic cigarette smoking on cerebral perfusion: a preliminary magnetic resonance study.

BACKGROUND: Although approximately 80% of individuals with alcohol use disorders are chronic smokers and despite reported associations between chronic cigarette smoking and lower cerebral perfusion in nonalcoholics, previous brain perfusion studies with alcoholics did not account for the potential effects of concurrent chronic cigarette smoking. METHODS: One-week-abstinent alcohol-dependent individuals in treatment (ALC) [19 smokers (sALC) and 10 nonsmokers (nsALC)] and 19 healthy light drinking, nonsmoking control participants (nsLD) were scanned with a pulsed arterial spin labeling method to measure cerebral perfusion without an exogenous contrast agent. Studies were performed with 2 different postlabeling delay times (time from labeling pulse to the excitation pulse; PLD=1,500 ms and PLD=1,200 ms) to assess the potential effect of arterial blood transit time on the perfusion. Average gray matter (GM) and white matter (WM) perfusion for the frontal and parietal lobes were calculated for each hemisphere from voxels containing at least 90% GM and 100% WM. RESULTS: At PLD=1,500 ms, multivariate analyses compared ALC (combined sALC and nsALC) with nsLD (p=0.04) and contrasted sALC, nsALC, and nsLD (p=0.006). ALC, as a group, showed 13% lower frontal GM perfusion (p=0.005) and 8% lower parietal GM perfusion than nsLD (p=0.03). With ALC separated into smokers and nonsmokers, sALC showed 19% lower frontal GM perfusion (p=0.001) and 12% lower parietal GM perfusion than nsLD (p=0.004). In sALC, a higher number of cigarettes smoked per day was associated with lower perfusion. Overall, regional perfusion did not differ significantly between nsALC and nsLD. Results obtained with PLD=1,200 ms generally confirmed the 1,500 ms findings. CONCLUSIONS: This study provides preliminary evidence that chronic cigarette smoking adversely affects cerebral perfusion in frontal and parietal GM of 1-week-abstinent alcohol-dependent individuals. These results are in line with our spectroscopic and structural magnetic resonance studies that suggest chronic cigarette smoking compounds the detrimental effects of alcohol dependence on brain neurobiology.

Brain metabolite concentrations and neurocognition during short-term recovery from alcohol dependence: Preliminary evidence of the effects of concurrent chronic cigarette smoking.

BACKGROUND: Longitudinal studies of brain tissue metabolite recovery in short-term abstinent alcoholics have primarily investigated the frontal lobes and cerebellum with variable results. Preliminary proton magnetic resonance spectroscopic imaging (1H MRSI) suggested that chronic cigarette smoking exacerbates alcohol-induced brain injury in 1-week abstinent alcoholics. However, the potential effects of chronic cigarette smoking on the recovery of alcohol-induced brain injury have not been studied. METHODS: Multislice short-echo time 1H MRSI was used to measure longitudinal changes in common brain metabolites in 25 recovering alcohol-dependent individuals (RA), retrospectively assigned to smoking (n = 14) and nonsmoking (n = 11) subgroups. Recovering alcohol-dependent individuals in longitudinal analyses were studied after approximately 7 and 34 days of abstinence from alcohol. In cross-sectional analyses, 36 RA (19 smokers, 17 nonsmokers) with approximately 34 days of sobriety were compared with 29 light drinkers (LD). Relationships between neurocognition and metabolite concentrations in abstinent RA were also examined. RESULTS: Over 1 month of abstinence from alcohol, RA, as a group, showed significant increases of regional N-acetylaspartate (NAA; marker of neuronal viability) and choline-containing compounds (Cho; marker of cell membrane synthesis/turnover) primarily in frontal and parietal lobes. These increases appeared to be driven by nonsmoking RA. Cross-sectional results indicate that metabolite levels in RA at 35 days of sobriety are not significantly different from those in LD in most regions, except for lower NAA and Cho in parietal WM and subcortical structures. However, metabolite levels at that time appear to be strongly modulated by smoking status. The patterns of metabolite-neurocognition relationships were different for nonsmoking and smoking RA. CONCLUSIONS: Within the first weeks of sobriety, regional brain NAA and Cho levels increased, but metabolite levels did not normalize in all brain regions after 35 days of sobriety. Neurobiologic recovery in RA appeared to be adversely affected by chronic smoking. Greater consideration of the effects of continued cigarette smoking on the neurobiologic and neurocognitive recovery of alcohol-dependent individuals is warranted.

Cigarette smoking exacerbates chronic alcohol-induced brain damage: a preliminary metabolite imaging study.

BACKGROUND: Cigarette smoking is common among alcohol-dependent individuals. Nevertheless, previous research has typically not accounted for the potential independent or compounding effects of cigarette smoking on alcohol-induced brain injury and neurocognition. METHODS: Twenty-four 1-week-abstinent recovering alcoholics (RAs; 14 smokers and 10 nonsmokers) in treatment and 26 light-drinking controls (7 smokers and 19 nonsmokers) were compared on measures of common brain metabolites in gray matter and white matter of the major lobes, basal ganglia, midbrain, and cerebellar vermis, obtained via multislice short-echo time proton magnetic resonance spectroscopic imaging. Smoking and nonsmoking RAs were also contrasted on measures of neurocognitive functioning, as well as laboratory markers of drinking severity and nutritional status. RESULTS: Chronic alcohol dependence, independent of smoking, was associated with lower concentrations of frontal N-acetylaspartate (NAA) and frontal choline-containing compounds, as well as lower parietal and thalamic choline. Smoking RAs had lower NAA concentrations in frontal white matter and midbrain and lower midbrain choline than nonsmoking RAs. A four-group analysis of covariance also demonstrated that chronic cigarette smoking was associated with lower midbrain NAA and choline and with lower vermian choline. In smoking RAs, heavier drinking was associated with heavier smoking, which correlated with numerous subcortical metabolite abnormalities. The 1-week-abstinent smoking and nonsmoking RAs did not differ significantly on a brief neurocognitive battery. In smoking RAs, lower cerebellar vermis NAA was associated with poorer visuomotor scanning speed and incidental learning, and in nonsmoking RAs lower vermis NAA was related to poorer visuospatial learning and memory. CONCLUSIONS: These human in vivo proton magnetic resonance spectroscopic imaging findings indicate that chronic cigarette smoking exacerbates chronic alcohol-induced neuronal injury and cell membrane damage in the frontal lobes of RAs and has independent adverse effects on neuronal viability and cell membranes in the midbrain and on cell membranes of the cerebellar vermis. Higher smoking levels are associated with metabolite concentrations in select subcortical structures. Greater consideration of the potential effects of comorbid cigarette smoking on alcohol-induced brain damage and other diseases affecting the central nervous system is warranted.