Purpose: Early identification of prenatal alcohol exposure (PAE) and of those in need of services resulting from this exposure is an important public health concern. This study reviewed the existing literature on potential biomarkers and screening tools of PAE and its impact.
Search methods: Electronic databases were searched for articles published between January 1, 1996, and November 30, 2021, using the following search terms: ("fetal alcohol" or "prenatal alcohol" or "FASD" or "alcohol-related neurodevelopmental disorder" or "ARND" or "ND-PAE") and ("screening" or "identification" or "biomarker"). Duplicate articles were electronically eliminated. Titles and abstracts were reviewed for appropriateness, and selected articles were retrieved for further analysis. Additional articles were added that were referenced in the reviewed articles or identified from expert knowledge. Information about the characteristics of the sample, the biomarker or screening tool, and the predictive validity outcome data were abstracted. A narrative analysis of the studies was then performed on the data.
Search results: A total of 3,813 articles were initially identified, and 1,215 were removed as duplicates. Of the remaining articles, 182 were identified as being within the scope of the review based on title and abstract inspection, and 181 articles were successfully retrieved. Of these, additional articles were removed because they were preclinical (3), were descriptive only (13), included only self-report of PAE (42), included only mean group comparison (17), were additional duplicates (2), focused on cost analysis (9), missed predictive validity data (24), or for other reasons (23). The remaining articles (n = 48) were abstracted. An additional 13 manuscripts were identified from these articles, and two more from expert knowledge. A total of 63 articles contributed to the review.
Discussion and conclusions: Biomarkers and screening tools of PAE and its impact fall short of ideal predictive validity characteristics. Higher specificity than sensitivity was found for many of the biomarkers and screening tools used to identify PAE and its impact, suggesting that current methods continue to under-identify the full range of individuals impacted by PAE. Exceptions to this were found in recent investigations using microRNAs related to growth and vascular development, proteomic changes associated with PAE, and combinations of markers estimating levels of various cytokines. Replications of these findings are needed across other samples to confirm the limited data available. Future research on biomarkers and screening tools should attend to feasibility and scalability of implementation. This article also recommends a systematic process of evaluation to improve early identification of individuals impacted by PAE so that harm reduction and habilitative care efforts can be implemente
Purpose: This narrative review summarizes and synthesizes the clinical trials and randomized clinical trials that evaluated selected and targeted approaches to reducing preconception and prenatal alcohol exposure (PAE) and alcohol-exposed pregnancy (AEP) since 2011.
Search methods: A professional hospital librarian completed the primary search using strategies specified within this review, resulting in 94 records returned in PubMed, Ovid MEDLINE, Clinical Key, the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. The author completed two supplementary literature searches.
Search results: From the total of 238 records returned from the three searches, 217 records were eliminated. Elimination reasons included other medical problem (119); duplicate entry (34); no content/results (23); secondary analysis (16); focus on effects of PAE (9); treatment of childhood fetal alcohol spectrum disorders (FASD) (6); maternal risk factors (3); and other (7). The remaining 21 studies were included with four overarching themes: (1) case management efforts (n = 4); (2) preconception efforts to reduce AEP (n = 5); (3) motivational interviewing and screening, brief intervention, and referral to treatment (n = 2); and (4) use of technology to deliver the intervention (n = 10).
Discussion and conclusions: Case management and home visits did not appear to have strong current empirical support. Study limitations included small sample sizes and no comparison groups, whereas larger efforts did not demonstrate definitive advantages to justify this intensive approach. The studies of preconception efforts, all based on the Project CHOICES approach, had similar outcomes, with the reduction in AEP risk largely due to improved contraception in women of childbearing age who were sexually active and drank alcohol but were not pregnant. It is unknown whether these women refrained from alcohol use when they became pregnant. Two studies of motivational interviewing to reduce prenatal alcohol use did not demonstrate the efficacy of the intervention. Both were small, with less than 200 pregnant women combined; moreover, the study samples had low baseline levels of alcohol use, allowing little opportunity for improvement. Finally, studies evaluating the impact of technological approaches to reducing AEP were reviewed. These exploratory investigations had small sample sizes and provided preliminary evaluations of techniques such as text messages, telephone contact, computer-based screening, and motivational interviewing. The potentially promising findings may inform future research and clinical efforts. Future directions may include research to address the limitations of the evidence to date and should reflect the complexities of FASD that include the biological and social context associated with prenatal alcohol use.
This article is part of a Festschrift commemorating the 50th anniversary of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Established in 1970, first as part of the National Institute of Mental Health and later as an independent institute of the National Institutes of Health, NIAAA today is the world's largest funding agency for alcohol research. In addition to its own intramural research program, NIAAA supports the entire spectrum of innovative basic, translational, and clinical research to advance the diagnosis, prevention, and treatment of alcohol use disorder and alcohol-related problems. To celebrate the anniversary, NIAAA hosted a 2-day symposium, "Alcohol Across the Lifespan: 50 Years of Evidence-Based Diagnosis, Prevention, and Treatment Research," devoted to key topics within the field of alcohol research. This article is based on Dr. Tapert's presentation at the event. NIAAA Director George F. Koob, Ph.D., serves as editor of the Festschrift.
Purpose: The purpose of this review is to discuss the literature regarding the concurrent use (co-use) of alcohol and cannabis and competing hypotheses as to whether cannabis acts as a substitute for (i.e., replacing the effects of alcohol, resulting in decreased use) or a complement to (i.e., used to enhance the effects of alcohol, resulting in increased use) alcohol. The impact of cannabis use on alcohol-related outcomes has received increased attention in the wake of ongoing legalization of cannabis for both medical and recreational purposes. Evidence for both hypotheses exists in the literature across a broad range of data collection methods and samples and is carefully reviewed here. In addition, various mechanisms by which cannabis may act as an alcohol substitute or complement are explored in depth with the goal of better understanding equivocal findings.
Search methods: This review includes articles that were identified from a search for studies on alcohol and cannabis co-use, with a specific focus on studies exploring complementary versus substitution aspects of co-use. Search terms were included in Google Scholar, PsycINFO, MEDLINE, and Web of Science. Eligible studies were those that measured alcohol and cannabis co-use in human samples in laboratory, survey, or ecological momentary assessment studies, or that directly referenced substitution or complementary patterns of use.
Search results: Search results returned 650 articles, with 95 meeting inclusion criteria.
Discussion and conclusions: Results of this review reveal compelling evidence for both substitution and complementary effects, suggesting nuanced yet significant distinctions across different populations examined in these studies. Several mechanisms for the impact of cannabis use on alcohol-related outcomes are identified, including patterns and context of co-use, timing and order of use, cannabinoid formulation, pharmacokinetic interactions, and user characteristics (including diagnostic status), all of which may influence substitution versus complementary effects. This review will inform future research studies examining this topic in both clinical and community samples and aid in the development of treatment and prevention efforts targeting those populations most vulnerable to negative consequences of co-use. Finally, this review highlights the need for additional research in more diverse samples and the use of mixed-methods designs to examine both pharmacological and contextual influences on co-use.
This article is part of a Festschrift commemorating the 50th anniversary of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Established in 1970, first as part of the National Institute of Mental Health and later as an independent institute of the National Institutes of Health, NIAAA today is the world's largest funding agency for alcohol research. In addition to its own intramural research program, NIAAA supports the entire spectrum of innovative basic, translational, and clinical research to advance the diagnosis, prevention, and treatment of alcohol use disorder and alcohol-related problems. To celebrate the anniversary, NIAAA hosted a 2-day symposium, "Alcohol Across the Lifespan: 50 Years of Evidence-Based Diagnosis, Prevention, and Treatment Research," devoted to key topics within the field of alcohol research. This article is based on Dr. Charness' presentation at the event. NIAAA Director George F. Koob, Ph.D., serves as editor of the Festschrift.
Purpose: The liberalization of cannabis policies has the potential to affect the use of other substances and the harms from using them, particularly alcohol. Although a previous review of this literature found conflicting results regarding the relationship between cannabis policy and alcohol-related outcomes, cannabis policies have continued to evolve rapidly in the years since that review.
Search methods: The authors conducted a narrative review of studies published between January 1, 2015, and December 31, 2020, that assessed the effects of cannabis policies on the use of alcohol in the United States or Canada.
Search results: The initial search identified 3,446 unique monographs. Of these, 23 met all inclusion criteria and were included in the review, and five captured simultaneous or concurrent use of alcohol and cannabis.
Discussion and conclusions: Associations between cannabis policy liberalization and alcohol use, alcohol-related outcomes, and the co-use of alcohol and cannabis were inconclusive, with studies finding positive associations, no associations, and negative associations. Although several studies found that cannabis policy liberalization was associated with decreases in alcohol use measures, these same studies showed no impact of the cannabis policy on cannabis use itself. The lack of a consistent association was robust to subject age, outcome measure (e.g., use, medical utilization, driving), and type of cannabis policy; however, this may be due to the small number of studies for each type of outcome. This paper discusses several notable limitations of the evidence base and offers suggestions for improving consistency and comparability of research going forward, including a stronger classification of cannabis policy, inclusion of measures of the alcohol policy environment, verification of the impact of cannabis policy on cannabis use, and consideration of mediation effects.
Purpose: A growing body of evidence has implicated the endocannabinoid (eCB) system in the acute, chronic, and withdrawal effects of alcohol/ethanol on synaptic function. These eCB-mediated synaptic effects may contribute to the development of alcohol use disorder (AUD). Alcohol exposure causes neurobiological alterations similar to those elicited by chronic cannabinoid (CB) exposure. Like alcohol, cannabinoids alter many central processes, such as cognition, locomotion, synaptic transmission, and neurotransmitter release. There is a strong need to elucidate the effects of ethanol on the eCB system in different brain regions to understand the role of eCB signaling in AUD.
Search methods: For the scope of this review, preclinical studies were identified through queries of the PubMed database.
Search results: This search yielded 459 articles. Clinical studies and papers irrelevant to the topic of this review were excluded.
Discussion and conclusions: The endocannabinoid system includes, but is not limited to, cannabinoid receptors 1 (CB1), among the most abundantly expressed neuronal receptors in the brain; cannabinoid receptors 2 (CB2); and endogenously formed CB1 ligands, including arachidonoylethanolamide (AEA; anandamide), and 2-arachidonoylglycerol (2-AG). The development of specific CB1 agonists, such as WIN 55,212-2 (WIN), and antagonists, such as SR 141716A (rimonabant), provide powerful pharmacological tools for eCB research. Alcohol exposure has brain region-specific effects on the eCB system, including altering the synthesis of endocannabinoids (e.g., AEA, 2-AG), the synthesis of their precursors, and the density and coupling efficacy of CB1. These alcohol-induced alterations of the eCB system have subsequent effects on synaptic function including neuronal excitability and postsynaptic conductance. This review will provide a comprehensive evaluation of the current literature on the synaptic interactions of alcohol exposure and eCB signaling systems, with an emphasis on molecular and physiological synaptic effects of alcohol on the eCB system. A limited volume of studies has focused on the underlying interactions of alcohol and the eCB system at the synaptic level in the brain. Thus, the data on synaptic interactions are sparse, and future research addressing these interactions is much needed.
This article is part of a Festschrift commemorating the 50th anniversary of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Established in 1970, first as part of the National Institute of Mental Health and later as an independent institute of the National Institutes of Health, NIAAA today is the world's largest funding agency for alcohol research. In addition to its own intramural research program, NIAAA supports the entire spectrum of innovative basic, translational, and clinical research to advance the diagnosis, prevention, and treatment of alcohol use disorder and alcohol-related problems. To celebrate the anniversary, NIAAA hosted a 2-day symposium, "Alcohol Across the Lifespan: 50 Years of Evidence-Based Diagnosis, Prevention, and Treatment Research," devoted to key topics within the field of alcohol research. This article is based on Dr. Sinha's presentation at the event. NIAAA Director George F. Koob, Ph.D., serves as editor of the Festschrift.
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