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BackgroundThe US Food and Drug Administration recently issued an advanced notice of proposed rule-making for reducing the nicotine content in cigarettes to a minimally addictive level. Very little is known about whether use of very low nicotine content (VLNC) cigarettes affects support for a nicotine reduction policy.ObjectiveThis study examined the effects of using VLNC versus usual brand (UB) cigarettes on support for a nicotine reduction policy and determined whether participant characteristics and responses to VLNC cigarettes were associated with policy support.MethodsParticipants from a cigarette trial who were assigned to either 0.4 mg nicotine/g tobacco research cigarettes or their UB for 6 weeks were asked about their support for the policy. χ2tests were used to compare support for the policy between cigarette conditions and logistic regression analyses were conducted to assess covariates associated with policy support.FindingsPolicy support did not differ by condition. After 6 weeks of using VLNC cigarettes, 50% of participants supported the policy, 26% opposed and 24% responded ‘Don’t Know’. Support was higher among those adherent to smoking only VLNC cigarettes (65%) compared with those who were non-adherent (44%). Older participants and those interested in quitting had increased odds of support. Cigarette satisfaction, perceived harm and perceived nicotine content were not significantly associated with support.ConclusionsSmoking VLNC cigarettes did not affect support for a nicotine reduction policy. Understanding predictors of policy support and opposition will help public health officials to maximise the public health acceptance and impact of this policy (ClinicalTrials.gov Identifier: NCT01681875 Post-Results).

Reducing the nicotine content in cigarettes could improve public health by reducing smoking and toxicant exposure, but may also have unintended consequences on alcohol use. The primary objective of this study was to examine the effect of reducing the nicotine content in cigarettes on alcohol outcomes. The secondary aim was to examine whether the effects of these cigarettes on alcohol outcomes were mediated by changes in nicotine exposure, smoking behavior, or withdrawal. Between June 2013 and July 2014, we conducted a 7‐arm, double‐blind, randomized clinical trial at 10 U.S.‐based sites. Daily smokers not currently interested in quitting (n = 839) were assigned to equally sized groups to smoke for 6 weeks cigarettes containing either normal nicotine content (NNC; 15.8 mg/g, 9 mg tar), moderate nicotine content (5.2 mg/g nicotine, 9 mg tar), or very low nicotine content (VLNC; 0.4 to 2.4 mg/g, 9 to 13 mg tar). This investigation focused on a subsample of current drinkers (n = 403). Each reduced nicotine content cigarette condition was compared to the NNCcontrol condition with respect to trajectories over the 6‐week period of average daily alcohol use and occurrence of binge drinking. Moderating variables were considered. Mediation analyses tested potential explanatory processes including changes in nicotine exposure, cigarettes per day, and withdrawal. Over time, reduced nicotine exposure and smoking rate mediated effects of VLNCcigarette use on reduced alcohol use. There was no evidence of compensatory drinking in response to nicotine reduction or nicotine withdrawal, even among subgroups expected to be at greater risk (e.g., relatively heavier drinkers, highly nicotine‐dependent individuals). The findings suggest that compensatory drinking is unlikely to occur in response to switching to VLNCcigarettes. In contrast, reducing the nicotine content of cigarettes may reduce alcohol use (clinicalTrials.gov number, NCT01681875). This study demonstrated that a reduced nicotine product standard could positively impact related health risk behaviors like drinking. Specifically, over time, reduced nicotine exposure, and smoking rate mediated effects of very low nicotine content (VLNC) cigarette use on reduced alcohol use. There was no evidence of compensatory drinking in response to nicotine reduction or nicotine withdrawal, even among subgroups expected to be at greater risk (e.g., relatively heavier drinkers, highly nicotine‐dependent individuals). Note. Abbreviations include TNE (total nicotine equivalents), CPD (cigarettes per day), BSL (baseline), WK (Week), and VLNC (very low nicotine content cigarettes). The change in alcohol use and cigarettes per day from baseline to Week 2, and Week 2 to Week 6 were estimated using piecewise latent growth curve models. The resulting model demonstrated adequate fit (χ2= 478.80, p < 0.001, RMSEA = 0.07 (90% CI: 0.06, 0.08), CFI: 0.95, TFI: 0.94). Several variables and pathways were excluded from the diagram to simplify the figure, including: intercepts of cigarettes per day and alcohol use which were allowed to correlate with each other and predicted the slope terms of the parallel process; baseline TNE which was included as a covariate for the effects of VLNC cigarettes on Week 2 and 6 TNE as well as the effects of Week 2 and Week 6 TNE on change in alcohol use; and the relations of all other covariates with TNE, changes in cigarettes per day, and alcohol use including gender, FTND score (minus CPD), minority status, and age.

Background: Naltrexone (NTX) has proven to be effective with alcoholics in treatment, with most controlled clinical trials showing beneficial effects on heavy drinking rates. However, little is known about the behavioral mechanisms underlying the effects of NTX on drinking, or about patient characteristics that may moderate NTX’s effects on drinking. In this study, ecological momentary assessment (EMA) techniques were used to investigate some of the putative mechanisms of naltrexone’s effects on drinking in heavy drinkers who were not seeking treatment for alcohol problems. Polymorphisms in the D4 dopamine receptor (DRD4) gene and the μ‐opiate receptor (OPRM1) gene, family history of alcohol problems, age of onset of alcoholism and gender were explored as potential moderators of NTX’s effects.

Exposure to various aversive stimuli (‘stressors’) as well as positively-reinforcing stimuli has been shown to increase extracellular dopamine concentrations in terminal areas of the mesocorticolimbic dopamine system. The magnitude and site specificity of the dopaminergic response may depend on the nature of the aversive stimulus. In the present study, in vivo microdialysis was used to examine the effects of an ethologically relevant stressor, namely threat of social defeat, on dopamine concentrations in nucleus accumbens, striatum, and prefrontal cortex of freely-moving male Long-Evans rats. During the test session, dialysate and video recording samples were collected from previously-defeated ‘intruder’ rats in consecutive phases, while (1) in the home cage, (2) when placed in the empty, soiled cage of a resident rat which had previously defeated them, (3) when exposed to threat of defeat by the resident, and (4) when returned to their home cages. Control animals were not defeated; in this group of rats video recording and dialysate samples were obtained when they were placed into an empty, clean novel cage and later returned to their home cage. The results indicated that levels of dopamine were elevated to approximately 130% of baseline in nucleus accumbens and prefrontal cortex when rats were placed into either the resident or novel cage. In defeated intruders, extracellular dopamine levels in accumbens and prefrontal cortex were increased further (approximately 160% of baseline), during social threat; these biochemical changes were synchronous with high levels of orienting toward the resident but not with heightened motor activity. Extracellular dopamine levels in lateral striatum were not affected by either manipulation. These results suggest that altered accumbens and cortical extracellular dopamine concentrations during social threat are not secondary to motor activation but instead reflect increased attention to the provocative stimulus or attempts by the intruder to ‘cope’ with the stimulus.

The high prevalence of cigarette smoking and tobacco related morbidity and mortality in people with chronic mental illness is well documented. This review summarizes results from studies of smoking cessation treatments in people with schizophrenia, depression, anxiety disorders, and post-traumatic stress disorder. It also summarizes experimental studies aimed at identifying biopsychosocial mechanisms that underlie the high smoking rates seen in people with these disorders. Research indicates that smokers with chronic mental illness can quit with standard cessation approaches with minimal effects on psychiatric symptoms. Although some studies have noted high relapse rates, longer maintenance on pharmacotherapy reduces rates of relapse without untoward effects on psychiatric symptoms. Similar biopsychosocial mechanisms are thought to be involved in the initiation and persistence of smoking in patients with different disorders. An appreciation of these common factors may aid the development of novel tobacco treatments for people with chronic mental illness. Novel nicotine and tobacco products such as electronic cigarettes and very low nicotine content cigarettes may also be used to improve smoking cessation rates in people with chronic mental illness.