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Background: Before the COVID‐19 pandemic, very little was known about the impact of social isolation on individuals' alcohol use and misuse. This study examines how socially isolated individuals with a history of heavy drinking used alcohol during the pandemic. Methods: Data for this study came from an add‐on to the Managing Heavy Drinking (MHD) longitudinal study of drivers convicted of DWI that was conducted in Erie County, New York. Pre‐COVID information (October 2019–March 2020) was augmented with a COVID‐19 questionnaire collected between July and August 2020. A total of 92 participants completed the COVID‐19 survey. Results: The sample of problem drinkers showed a significant increase after the pandemic outbreak in the average number of drinking days from 1.99 to 2.49 per week (p = 0.047), but a significant decrease in the average number of drinks per drinking day, from 3.74 to 2.74 (p = 0.003). The proportion of individuals who drank more frequently was greater among those who, before the outbreak had an Alcohol Use Disorders Identification Test (AUDIT) score <8 (26% increase) compared with those with an AUDIT score of >8 (13%). Alcohol treatment was also associated with the frequency of drinking, with individuals who were not in alcohol treatment showing a 16% increase in frequency compared with a 10% increase among those in treatment. Further, individuals who, after the outbreak worried about their health (30%) or finances (37%) reported greater increases in the frequency of drinking than those who did not worry about their health (17%) or finances (10%). Conclusions: Overall, the individuals in our sample showed small changes in the frequency andheaviness of drinking after the outbreak of COVID‐19, effects that opposite in direction from one another and thus resulted in no overall change in drinks consumed. Nonetheless, we identified factors that influenced the effects of the pandemic on drinking behavior among individuals convicted of DWI, which emphasizes the need to individualize these individuals' treatment, particularly in the context of dramatic environmental change. [ABSTRACT FROM AUTHOR]

Background: Half of the offenders convicted of impaired driving in the United States are sentenced to install alcohol ignition interlock devices (IIDs), which prevent them from starting their vehicles if they have been drinking. No research has yet explored offenders' patterns of alcohol consumption and driving under the influence of alcohol (DUI) from the time before the arrest to the time period after the IID is installed. This study aims to fill that gap in knowledge. Methods: Using the Timeline Follow‐back interview procedure, we assessed the daily drinking of 153 convicted DUI offenders' self‐reported total alcohol consumption and rates of self‐reported driving after drinking over 4 phases: before DUI arrest, between arrest and IID installation, during the phase on the interlock, and after the interlock is removed. Because information about behaviors in each period was not available for every participant, comparisons were made using paired‐sample contrasts. Results: Compared with before the arrest, total alcohol use decreased by 50% in the 4‐month phase following arrest and before IID installation, though it did not change much afterward. The frequency of drinking and driving decreased sharply after the arrest (−82%), with further decrease upon installation of the interlock (−58%, p = 0.05). The frequency of drinking and driving after the IID was removed returned to preinstallation drinking and driving status (+58%, p = 0.01). Conclusions: Participants made significant adjustments to their drinking behavior by adhering to the traditional DUI driving restrictions in the postarrest phase. Although installation of an IID was not associated with a significant change in drinking, it further reduced the frequency of drinking and driving. Evaluations of the IID experience should take into account information on an individual's drinking and DUI behaviors not only before the IID was installed, but before the individual was arrested. [ABSTRACT FROM AUTHOR]

Background: Teens who delay driving licensure may not be subject to graduated driver licensing restrictions that are known to reduce crash risk. We explored the association of delay in licensure with driving while impaired (DWI) and riding with an impaired driver (RWI) among emerging adults. Methods: Data from the NEXT Generation Health Study, starting with 10th grade (2009–2010), were analyzed. The outcome variables were Wave 7 (W7) self‐reported DWI and RWI as dichotomous variables. The independent variable was delay in licensure. Covariates included sex, urbanicity, race/ethnicity, family structure, parent education, family affluence, teen's highest education, minimum legal drinking age laws, and onset age of alcohol use. Descriptive analysis and logistic regressions were conducted. Results: Of 2525 participants eligible for licensure, 887 reported a delay in licensure by 1–2 years (38.9%, weighted) and 1078 by > 2 years (30.3% weighted) across 7 waves. In W7, 23.5% (weighted and hereafter, 5.6% once, 17.8% ≥twice) of participants reported DWI and 32.42% (5.6% once, 25.4% ≥twice) reported RWI. Logistic regressions showed no overall significant association of delay in licensure with either W7 RWI or W7 DWI. However, in stratified analyses, among African American youth, delay in licensure was positively associated with DWI (OR = 2.41, p = 0.03) and RWI (OR = 2.72, p = 0.05). Among those with ≤ high school or lower education by W7, delayed licensure was positively associated with RWI (OR = 2.51, p < 0.01). Conclusions: While in the overall sample, delayed licensure did not appear to be associated with DWI or RWI, our findings suggest that delayed licensure may be of concern to teen risk of DWI and RWI among African Americans and among those with lower educational attainment. Furthermore, as two‐thirds of youth delayed licensure, more research is needed to determine whether this is more of a positive (i.e., protective) factor by reducing their exposure to crash risk or a negative (i.e., risk) factor due to their missing important driver safety stages of graduated driver licensing. The recent phenomena of teen delay in driving licensure (DDL) among U.S. high school students is prevalent and persists. Questions around DDL on the safety of more vulnerable teens exist when it comes to its potential effects on later driving while impaired and riding with an impaired driver. Among African American teens and teens overall with lower education attainment, delaying licensure may put these youth at risk for later driving while impaired and riding with an impaired driver. [ABSTRACT FROM AUTHOR]

The influence of ethanol on cardiac lipid metabolism has been investigated in the rat. Acute in vitro ethanol significantly stimulated the incorporation of 14C-1-acetate but not 14C-U-glucose into cardiac lipid in rats fed a diet free of ethanol for 3 weeks. Stimulation of incorporation was not uniform but was confined to the diglyceride and triglyceride fractions. This response of cardiac tissue lipid metabolism to acute ethanol was not observed in rats pair fed an isocaloric diet containing 36% of calories as ethanol. Chronic ethanol feeding significantly increased cardiac triglyceride content when compared with pair-fed controls. It also stimulated oxidation of labeled palmitate, but did not affect in vitro lipogenesis. [ABSTRACT FROM AUTHOR]

Background: Riding with a drinking driver (RWDD) is a serious concern that leads to numerous preventable deaths every year. There is a significant gap in research on empirically tested predictors of RWDD that could be implemented in prevention efforts. College students are in need of such prevention efforts, as they have some of the highest rates of alcohol‐related crash fatalities and may engage in RWDD more than their noncollege peers. This study utilized behavioral decision‐making approach to examine predictors of RWDD and declining a ride from a drinking driver (Decline) in older college students. Methods: Students (n = 791) in their third year of college were enrolled from 3 large and diverse universities. Psychosocial (e.g., expectancies, norms) and decision‐making variables (willingness to RWDD and intentions to use alternatives) were assessed in the fall of their third year. One year later, RWDD and Decline behaviors were assessed. Zero‐inflated Poisson analyses were used to assess how decision‐making variables predicted RWDD and Decline behavior. Associations between psychosocial and decision‐making variables were also assessed. Results: Thirteen percent of students reported RWDD and ~28% reported Decline behavior. Willingness to RWDD and typical weekly drinking were both associated with increases in RWDD (odds ratio [OR] = 1.58 and 1.40, respectively), whereas intentions to use alternatives, sex, and ethnicity were not associated with RWDD. Only weekly drinking was associated with Decline, with an increase in drinking associated with increased Decline (OR = 1.48). All psychosocial variables were significantly associated with the decision‐making variables except positive expectancies. Conclusions: Results provide evidence that willingness to RWDD is a predictor of future RWDD, even if students intend to use safe alternatives. Future research is needed to better understand decision‐making factors that influence Decline. Results also suggest prevention and interventions efforts, such as brief motivational intervention, Parent‐Based Interventions, and normative feedback interventions could be adapted to reduce RWDD. [ABSTRACT FROM AUTHOR]

Background Chronic pancreatitis, a known complication of alcohol abuse, is characterized histopathologically by prominent fibrosis. Pancreatic stellate cells ( PSCs) are responsible for producing this fibrous tissue in chronic pancreatitis and are activated by alcohol. Progression of alcoholic chronic pancreatitis (as assessed by calcification and fibrosis) is thought to be facilitated by concurrent smoking, but the mechanisms are unknown. This study aimed to (a) determine whether human PSCs (hPSCs) and rat PSCs express nicotinic acetylcholine receptors ( nAChRs), which are known to bind 2 important components of cigarette smoke, namely nicotine and nicotine-derived nitrosamine ketone ( NNK), and (b) examine the effects of cigarette smoke components in the presence and absence of alcohol on PSC activation in vitro. Methods Western blotting was used to detect the presence of nAChRs in primary cultures of PSCs. Clinically relevant concentrations of cigarette smoke components (either cigarette smoke extract [ CSE], NNK, or nicotine) ± ethanol (EtOH) were used to treat primary cultures of PSCs, and stellate cell activation was assessed by cell migration, proliferation, collagen production, and apoptosis. Results We demonstrate, for the first time, that PSCs express nAChRs (isoforms α3, α7, β, ε) and that the expression of the α7 isoform in hPSCs is induced by CSE + EtOH. We also provide novel findings that PSCs are activated by CSE and NNK (both alone and in combination with EtOH) as evidenced by an increase in cell migration and/or proliferation. Further, we demonstrate that activation of PSCs by CSE + EtOH and NNK + EtOH may be mediated via nAChRs on the cells. Conclusions PSCs are activated by clinically relevant concentrations of cigarette smoke components ( CSE and NNK), alone and in combination with EtOH. Thus, in alcoholics who smoke, progression of pancreatic fibrosis may be facilitated by the combined effects of alcohol and cigarette smoke components on hPSC behavior. [ABSTRACT FROM AUTHOR]

Background: Access to specialty alcoholism treatment in rural environments is limited and new treatment approaches are needed. The objective was to evaluate the efficacy of naltrexone alone and in combination with sertraline among Alaska Natives and other Alaskans living in rural settings. An exploratory aim examined whether the Asn40Asp polymorphism of the μ-opioid receptor gene ( OPRM1) predicted response to naltrexone, as had been reported in Caucasians. Methods: Randomized, controlled trial enrolling 101 Alaskans with alcohol dependence, including 68 American Indians/Alaska Natives. Participants received 16 weeks of either (1) placebo (placebo naltrexone + placebo sertraline), (2) naltrexone monotherapy (50 mg naltrexone + sertraline placebo) and (3) naltrexone + sertraline (100 mg) plus nine sessions of medical management and supportive advice. Primary outcomes included Time to First Heavy Drinking Day and Total Abstinence. Results: Naltrexone monotherapy demonstrated significantly higher total abstinence (35%) compared with placebo (12%, p = 0027) and longer, but not statistically different, Time to First Heavy Drinking Day ( p = 0.093). On secondary measures, naltrexone compared with placebo demonstrated significant improvements in percent days abstinent ( p = 0.024) and drinking-related consequences ( p = 0.02). Combined sertraline and naltrexone did not differ from naltrexone alone. The pattern of findings was generally similar for the American Indian/Alaska Native subsample. Naltrexone treatment response was significant within the group of 75 individuals who were homozygous for OPRM1 Asn40 allele. There was a small number of Asp40 carriers, precluding statistical testing of the effect of this allele on response. Conclusions: Naltrexone can be used effectively to treat alcoholism in remote and rural communities, with evidence of benefit for American Indians and Alaska Natives. New models of care incorporating pharmacotherapy could reduce important health disparities related to alcoholism. [ABSTRACT FROM AUTHOR]

This article represents the proceedings of a workshop at the 2000 ISBRA Meeting in Yokohama, Japan. The presentations were (1) Phenotypic alteration of myofibroblast during ethanol-induced pancreatic injury: its relation to bFGF, by Masahiko Nakamura, Kanji Tsuchimoto, and Hiromasa Ishii; (2) Activation of pancreatic stellate cells in pancreatic fibrosis, by Paul S. Haber, Gregory W. Keogh, Minoti V. Apte, Corey S. Moran, Nancy L. Stewart, Darrell H.G. Crawford, Romano C. Pirola, Geoffrey W. McCaughan, Grant A. Ramm, and Jeremy S. Wilson; (3) Pancreatic blood flow and pancreatic enzyme secretion on acute ethanol infusion in anesthetized RAT, by H. Nishino, M. Kohno, R. Aizawa, and N. Tajima; (4) Genotype difference of alcohol-metabolizing enzymes in relation to chronic alcoholic pancreatitis between the alcoholic in the National Institute on Alcoholism and patients in other general hospitals in Japan, by K. Maruyama, H. Takahashi, S. Matsushita, K. Okuyama, A. Yokoyama, Y. Nakamura, K. Shirakura, and H. Ishii; and (5) Alcohol consumption and incidence of type 2 diabetes, by Katherine M. Conigrave, B. Frank Hu, Carlos A. Camargo Jr, Meir J. Stampfer, Walter C. Willett, and Eric B. Rimm. [ABSTRACT FROM AUTHOR]

Background: The observation that only a minority of alcoholics develops clinical pancreatic disease has led to a search for a predisposing factor to the disease. One possible predisposing factor is mutation of the cystic fibrosis transmembrane conductance regulator (CFTR) gene as cystic fibrosis leads to pancreatic injury. We have recently demonstrated that 15 common CFTR mutations are not found in patients with alcoholic pancreatitis. Another common polymorphism of the CFTR gene has recently been implicated in the pathogenesis of idiopathic chronic pancreatitis, the 5T variant of the variable length polythymidine tract in intron 8 (the normal genotypes are 7T and 9T). The 5T variant inhibits transcription of exon 9 resulting in a CFTR protein lacking chloride channel activity. The aim of this study was to determine whether the 5T variant is associated with alcoholic pancreatitis. Methods: Fifty-two patients with alcoholic pancreatitis were identified using standardized diagnostic criteria. Fifty alcoholics without pancreatitis were also studied as controls. Genomic DNA was extracted from peripheral blood leukocytes and the polythymidine tract of intron 8 was amplified by nested polymerase chain reaction using established primers. The polymerase chain reaction products were digested with Msel, separated by electrophoresis on 15% polyacrylamide gels and genotypes assigned by comparison with known positive controls. Results: The 5T allele was found in only two patients with alcoholic pancreatitis (3.9% of the index group; 95% confidence intervals 0-10%) and in seven alcoholic controls. Allele frequencies for 5T, 7T, and 9T in patients with alcoholic pancreatitis were 1.9%, 85.6%, and 12.5%, respectively. These did not differ from the allele frequencies in alcoholic controls (7%, 79%, and 14% for 5T, 7T, and 9T, respectively). Conclusion: The 5T allele was not associated with alcoholic pancreatitis. Individual susceptibility to this disease remains unexplained. [ABSTRACT FROM AUTHOR]