Background: Heterogeneity in the driving while impaired (DWI) offender population and modest outcomes from remedial programs are fueling interest in clarifying clinically significant DWI subtypes to better assess recidivism risk and target interventions. Our previous research identified 2 putative behavior phenotypes of DWI offenders with distinct behavioral, personality, cognitive, and neurobiological profiles: (i) offenders primarily engaging in DWI (pDWI); and (ii) offenders engaging in DWI and other traffic violations (MIXED). Here, we evaluate these phenotypes' clinical significance for prediction of recidivism and intervention targeting.
Methods: DWI recidivists participating in a previous randomized controlled trial (N = 184 comparing brief motivational interviewing (BMI) and an information and advice control condition (IA) were retrospectively classified as either pDWI (n = 97) or MIXED (n = 87). Secondary analyses then evaluated the effect of this phenotypic classification on self-reported 6- and 12-month alcohol misuse outcomes and documented 5-year DWI recidivism violations, and in response to either BMI or IA (i.e., pDWI-BMI, n = 46; MIXED-BMI, n = 45; pDWI-IA, n = 51; MIXED-IA, n = 42). Two hypotheses were tested: (i) MIXED classification is associated with poorer alcohol misuse outcomes and recidivism outcomes than pDWI classification; and (ii) pDWI paired with BMI is associated with better outcomes compared to MIXED paired with BMI.
Results: MIXED classification was associated with significantly greater risk of recidivism over the 5-year follow-up compared to pDWI classification. Moreover, the pDWI-BMI pairing was associated with significantly decreased recidivism risk compared to the MIXED-BMI pairing. Analyses of 6- and 12-month alcohol use outcomes produced null findings.
Conclusions: The clinical significance of phenotypic classification for risk assessment and targeting intervention was partially supported with respect to recidivism risk. Prospective investigation of this and other behavioral phenotypes is indicated.
Background: Brief interventions have empirical support for acutely reducing alcohol use among non-treatment-seeking heavy drinkers. Neuroimaging techniques allow for the examination of the neurobiological effect of behavioral interventions, probing brain systems putatively involved in clinical response to treatment. Few studies have prospectively evaluated whether psychosocial interventions attenuate neural cue reactivity that in turn reduces drinking in the same population. This study aimed to examine the effect of a brief intervention on drinking outcomes, neural alcohol cue reactivity, and the ability of neural alcohol cue reactivity to prospectively predict drinking outcomes.
Methods: Non-treatment-seeking heavy drinking participants were randomized to receive a brief interview intervention (n = 22) or an attention-matched control (n = 24). Immediately following the intervention or control, participants underwent a functional magnetic resonance imaging scan comprised of the alcohol taste cues paradigm. Four weeks after the intervention (or control), participants completed a follow-up visit to report on their past-month drinking. Baseline and follow-up percent heavy drinking days (PHDD) were calculated for each participant.
Results: There was no significant effect of the brief intervention on PHDD at follow-up or on modulating neural activation to alcohol relative to water taste cues. There was a significant association between neural response to alcohol taste cues and PHDD across groups (Z > 2.3, p < 0.05), such that individuals who had greater neural reactivity to alcohol taste cues in the precuneus and prefrontal cortex (PFC) had fewer PHDD at follow-up.
Conclusions: This study did not find an effect of the brief intervention on alcohol use in this sample, and the intervention was not associated with differential neural alcohol cue reactivity. Nevertheless, greater activation of the precuneus and PFC during alcohol cue exposure predicted less alcohol use prospectively suggesting that these neural substrates subserve the effects of alcohol cues on drinking behavior.
Background: Prenatal alcohol exposure (PAE) can result in permanent disability, including physical, neurodevelopmental, and cognitive impairments, known as fetal alcohol spectrum disorder (FASD). Individuals with FASD are more likely to engage with the law, including being placed in detention, than individuals without FASD. Young people who were sentenced to detention participated in a FASD prevalence study in Western Australia. The diagnosis of FASD requires a multidisciplinary assessment and confirmation of maternal alcohol consumption during pregnancy. Obtaining accurate assessment of PAE for young people participating in the study was challenging.
Methods: An interview with the birth mother or other responsible adult for young people sentenced to detention in Western Australia was conducted as part of the FASD assessment. The Alcohol Use Disorders Identification Test consumption subset (AUDIT-C), other relevant questions, and documentary evidence were used to assess PAE. PAE was categorized according to the Australian Guide to the Diagnosis of FASD: no PAE reported, confirmed or confirmed high-risk, or unknown.
Results: Among the 101 participants, information on PAE was unable to be obtained for 13 (13%) young people. Of the remaining 88 participants with information of PAE, 41 reported no PAE and 47 had confirmed PAE.
Conclusions: Accurately assessing prenatal alcohol consumption is challenging in any setting, but it is exceptionally challenging when assessed 13 to 17 years retrospectively as part of a FASD assessment for a young person sentenced to detention. Recording and recoding detailed qualitative responses was required to provide an accurate assessment of PAE using the AUDIT-C. Standardized recording of PAE in antenatal and birth records would facilitate later assessments for FASD and provide opportunities for advice and support for women who continue to drink during pregnancy.
Background: Alcohol abuse and adherence to atherogenic diet (AD; a low-carbohydrate-high-protein diet) have been positively associated with cardiovascular disease. In addition, it has been demonstrated clinically that dietary intake is increased on days when alcohol is consumed. Here, the additive effects of ethanol (EtOH) and AD on atherosclerosis, a major underlying cause of cardiovascular disease, were investigated in apolipoprotein E/low-density lipoprotein receptor double-knockout (KO) mice. The mechanisms, especially aortic oxidative stress damage, were highlighted.
Methods: Twelve-week-old male KO mice on AD with or without EtOH treatment were bred for 4 months. Age-matched male C57BL/6J mice on a standard chow diet without EtOH treatment served as controls. Analyses were conducted using ultrasound biomicroscopy, histopathological and fluorescence immunohistochemical examinations, Western blots, and polymerase chain reaction.
Results: KO mice on AD with EtOH treatment showed increases in aortic maximum intima media thickness, hypoechoic plaque formation, and mean Oil-Red-O content. These results were associated with enhanced ratio of aortic 8-hydroxy-2'-deoxyguanosine (8-OHdG)-immunopositive area to the metallothionein (MT) immunopositive area and suppression of AD-induced up-regulated aortic Mt1, Mt2, and upstream stimulatory factor 1 mRNA expressions. Moreover, 8-OHdG was expressed in the nuclei of CD31- and alpha smooth muscle actin-immunopositive cells, and the up-regulated mRNA expressions of aortic nitric oxide synthase 3 and platelet-derived growth factors were only observed in the KO mice on AD with EtOH treatment.
Conclusions: Alcohol abuse and adherence to AD may promote the shift of aortic oxidative stress and antioxidative stress balance toward oxidative stress predominance and reduced antioxidative stress, which may be partly due to the decrease in MT at the cell biological level and down-regulation of Mt at the gene level, which in turn could play a role in the up-regulation of endothelial dysfunction-related and vascular smooth muscle cell proliferation-related gene expression and the progression of atherosclerosis in mice with hyperlipidemia.
Background: Gestational ethanol (EtOH) exposure is associated with multiple developmental abnormalities, collectively termed fetal alcohol spectrum disorder (FASD). While the majority of women abstain from EtOH following knowledge of pregnancy, one contributing factor to the high FASD prevalence is that pregnancy is not detected until 4 to 6 weeks. Thus, EtOH consumption continues during the initial stages of fetal development.
Methods: An experimental protocol is described in which rhesus macaques self-administer 1.5 g/kg/d EtOH (or isocaloric maltose dextrin) prior to pregnancy and through the first 60 days of a 168-day gestation term. Menstrual cycles were monitored, including measurements of circulating estradiol and progesterone levels. The latency to consume 1.5 g/kg EtOH and blood EtOH concentration (BEC) was measured.
Results: Twenty-eight fetuses (14 EtOH and 14 controls) were generated in this study. EtOH did not affect menstrual cycles or the probability of successful breeding. No EtOH-induced gross adverse effects on pregnancy were observed. Individual variability in latency to complete drinking translated into variability in BEC, measured 90 minutes following session start. Drinking latencies in controls and EtOH drinkers were longer in the second gestational month than in the first. All pregnancies reached the planned experimental time point of G85, G110, or G135, when in utero MRIs were performed, fetuses were delivered by caesarean section, and brains were evaluated with ex vivo procedures, including slice electrophysiology. Fetal tissues have been deposited to the Monkey Alcohol Tissue Research Resource.
Conclusions: This FASD model takes advantage of the similarities between humans and rhesus macaques in gestational length relative to brain development, as well as similarities in EtOH self-administration and metabolism. The daily 1.5 g/kg dose of EtOH through the first trimester does not influence pregnancy success rates. However, pregnancy influences drinking behavior during the second month of pregnancy. Future publications using this model will describe the effect of early-gestation EtOH exposure on anatomical and functional brain development at subsequent gestational ages.
Background: Early initiation of alcohol drinking has been associated with increased risk of alcohol dependence in adulthood. Although negative affect mediated in part by corticotropin-releasing factor (CRF) is a strong motivator for alcohol consumption in adults, comparisons of alcohol withdrawal in adolescents and adults generally have not included CRF-related measures such as anxiety. The purpose of the present study was to compare withdrawal signs including anxiety-like behavior after a brief multiday alcohol treatment in adolescent and adult male and female rats.
Methods: Animals were treated with a 5-day regimen of alcohol injections (3 daily intraperitoneal injections of 1.5 g/kg at 3-hour intervals, total of 15) starting on postnatal day (PN) 28 or PN 70. Spontaneous withdrawal signs and anxiety-like behavior (light/dark box) were assessed 18 hours after the last injection as described. One cohort of rats was treated with alcohol, killed 18 hours after the last injection, and blood was collected to assess corticosterone. Another cohort of rats was treated with alcohol or vehicle, given 1, 2, or 3 alcohol injections (1.5 g/kg), and killed 1 hour after final injection to determine blood alcohol concentration (BAC). Finally, adult and adolescent males and females received 5 days of alcohol or vehicle treatment followed by a final challenge with alcohol (3 g/kg), and blood was collected for corticosterone.
Results: BAC was comparable in adolescents and adults. Spontaneous withdrawal signs were comparable in adolescents and adults, and no sex differences were observed. Anxiety-like behaviors (time and distance in light, latency to emerge, and light entries) differed in alcohol- and vehicle-treated adults but not adolescents. Corticosterone was not elevated at withdrawal. Alcohol increased corticosterone significantly in vehicle-treated animals, but both adolescents and adults were tolerant to alcohol-induced elevation of corticosterone after 5 days of alcohol treatment.
Conclusions: These findings suggest that adolescents experience milder negative affect during withdrawal from brief alcohol exposures relative to adults but comparable suppression of hypothalamic-pituitary-adrenal axis function.
Background: Studies of the role of alcohol use in diabetes risk have rarely included lifetime alcohol use measures, including the frequency of heavy occasions, or evaluated risks among Black or Hispanic respondents in US samples.
Methods: Data from the 2014 to 2015 National Alcohol Survey of the U.S. population were used to estimate diabetes risk from drinking patterns at the time of onset in Cox proportional hazards models in a retrospective cohort design. Models for the population, males and females, and for White, Black, and Hispanic respondents of both genders were estimated using 2 versions of drinking pattern groupings at each age.
Results: While a number of significant results were found with the first version of the drinking measures, we focus on those confirmed with measures from responses strictly prior to the age of risk estimation. Compared to the lifetime abstainer group, the "drinking at least weekly with less than monthly 5+" group had a significantly lower hazard ratio (HR) for the total sample (HR = 0.64) and among Whites (HR = 0.42). Significantly reduced risks were found in the same models for those who drank 5+ at least monthly but not weekly. No significantly elevated risks were found for either current or prior heavy occasion drinking.
Conclusions: These results are consistent with some prior studies in finding reduced risks for regular light-to-moderate drinkers, but not consistent with findings from other studies showing increased risk from heavy occasion drinking, particularly among women. New and larger studies with well-defined drinking pattern measures are needed, particularly for U.S. Blacks and Hispanics, to address varying results in this literature.
Background: Pancreatitis is an increasingly common clinical condition that causes significant morbidity and mortality. Cannabis use causes conflicting effects on pancreatitis development. We conducted a larger and more detailed assessment of the impact of cannabis use on pancreatitis.
Methods: We analyzed data from 2012 to 2014 of the Healthcare Cost and Utilization Project-Nationwide Inpatient Sample discharge records of patients 18 years and older. We used the International Classification of Disease, Ninth Edition codes, to identify 3 populations: those with gallstones (379,125); abusive alcohol drinkers (762,356); and non-alcohol-non-gallstones users (15,255,464). Each study population was matched for cannabis use record by age, race, and gender, to records without cannabis use. The estimation of the adjusted odds ratio (aOR) of having acute and chronic pancreatitis (AP and CP) made use of conditional logistic models.
Results: Concomitant cannabis and abusive alcohol use were associated with reduced incidence of AP and CP (aOR: 0.50 [0.48 to 0.53] and 0.77 [0.71 to 0.84]). Strikingly, for individuals with gallstones, additional cannabis use did not impact the incidence of AP or CP. Among non-alcohol-non-gallstones users, cannabis use was associated with increased incidence of CP, but not AP (1.28 [1.14 to 1.44] and 0.93 [0.86 to 1.01]).
Conclusions: Our findings suggest a reduced incidence of only alcohol-associated pancreatitis with cannabis use.
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