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BackgroundThere have been reports of increased alcohol consumption during the COVID-19 pandemic in the general population. However, little is known about the impact of the pandemic on the prevalence of alcohol use disorder (AUD), especially in high-risk samples such as U.S. military veterans.MethodsData were analyzed from the 2019-2020 National Health and Resilience in Veterans Study, which surveyed a nationally representative, prospective cohort of 3078 U.S. veterans. Pre-pandemic and 1-year peri-pandemic risk and protective factors associated with incident and chronic probable AUD were examined.ResultsA total of 6.9 % (n = 183) of veterans were classified as chronic probable AUD, 3.2 % (n = 85) as remitted from AUD, and 2.7 % (n = 71) as incident probable AUD during the pandemic; the prevalence of probable AUD in the full sample remained stable -10.1 % pre-pandemic and 9.6 % peri-pandemic. Younger age, greater pre-pandemic alcohol use severity, and COVID-related stressors were associated with incident AUD during the pandemic, whereas higher pre-pandemic household income was associated with lower risk of this outcome. Younger age, combat experience, lifetime substance use disorder, greater drug use severity, lower dispositional optimism, and more COVID-related worries and social restriction stress were associated with higher risk of chronic AUD.ConclusionsNearly 1-in-10 US veterans screened positive for AUD 1-year into the pandemic; however, the pre- and 1-year peri-pandemic prevalence of probable AUD remained stable. Veterans who are younger, have served in combat roles, endorse more COVID-related stressors, and have fewer socioeconomic resources may be at higher risk for AUD during the pandemic.

Background and Objectives: There are high rates of comorbidity between posttraumatic stress disorder (PTSD) and opioid use disorder (OUD). Evidence‐based trauma‐focused psychotherapies such as Cognitive Processing Therapy (CPT) are a first‐line treatment for PTSD. Veterans with OUD are treated primarily in substance use disorder (SUD) clinics where the standard of care is drug counseling; they often do not have access to first‐line PTSD treatments. This study tested whether CPT can be conducted safely and effectively in veterans with comorbid OUD treated with buprenorphine. Methods: This 12‐week, 2‐site, randomized clinical trial (RCT) included open‐label randomization to two groups: (a) CPT versus (b) Individual Drug Counselling (IDC) in veterans with PTSD and comorbid OUD who were maintained on buprenorphine (N = 38). Results: Veterans randomized to either IDC (n = 18) or CPT (n = 20) showed a significant reduction in self‐reported PTSD symptoms over time as measured by the PTSD checklist (PCL‐5) but there were no treatment group differences; there was some indication that reduction in PTSD symptoms in the CPT group were sustained in contrast to the IDC group. Recruitment was significantly impacted by COVID‐19 pandemic, so this study serves as a proof‐of‐concept pilot study. Discussion and Conclusions: Veterans with OUD and PTSD can safely and effectively participate in evidence‐based therapy for PTSD; further work should confirm that trauma‐focused treatment may be more effective in leading to sustained remission of PTSD symptoms than drug counseling. Scientific Significance: This is the first study to evaluate CPT for PTSD in the context of buprenorphine treatment for OUD. [ABSTRACT FROM AUTHOR]

Background and Objectives Methods Results Discussions and Conclusions Scientific Significance Noradrenergic dysregulation is important in the pathophysiology of posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD); pharmacotherapies targeting adrenergic function have potential as treatment for comorbidity. Dexmedetomidine (sublingual film formulation—BXCL501; IGALMI) is a highly potent, selective ⍺2‐adrenergic receptor agonist and may be superior to other pharmacotherapeutic approaches. A within subjects, phase 1b safety laboratory study was conducted to evaluate adverse effects of BXCL501 when combined with alcohol; BXCL501's potential efficacy was also explored.Heavy drinker participants with a diagnosis of or who were at risk for PTSD participated in three separate test days which included pretreatment with BXCL501 (40 µg, 80 µg or placebo) administered in a randomized, double‐blind fashion, followed by three testing conditions: alcohol cue reactivity, trauma‐induced reactivity, and IV ethanol administration. Safety outcomes included blood pressure (BP) and sedation. Exploratory outcomes included alcohol craving, trauma‐induced anxiety and craving and subjective effects of alcohol.Ten of twelve randomized participants competed the entire study. BXCL501 (80 µg) was associated with expected mild changes in BP and sedation; administration with alcohol did not affect those parameters. There were no clinically significant adverse effects. BXCL501 attenuated trauma‐induced anxiety and attenuated subjective effects of alcohol.BXCL501 is safe for use in humans who may drink alcohol while undergoing treatment. BXCL501 may be explored as a potential treatment for PTSD and AUD.This is the first study to provide scientific support for BXCL501's potential to treat PTSD and comorbid AUD. [ABSTRACT FROM AUTHOR]

Posttraumatic stress disorder (PTSD) is a chronic psychiatric condition that follows exposure to a traumatic stressor. Though previous in vivo proton (1H) MRS) research conducted at 4 T or lower has identified alterations in glutamate metabolism associated with PTSD predisposition and/or progression, no prior investigations have been conducted at higher field strength. In addition, earlier studies have not extensively addressed the impact of psychiatric comorbidities such as major depressive disorder (MDD) on PTSD‐associated 1H‐MRS‐visible brain metabolite abnormalities. Here we employ 7 T 1H MRS to examine concentrations of glutamate, glutamine, GABA, and glutathione in the medial prefrontal cortex (mPFC) of PTSD patients with MDD (PTSD+MDD+; N = 6) or without MDD (PTSD+MDD−; N = 5), as well as trauma‐unmatched controls without PTSD but with MDD (PTSD−MDD+; N = 9) or without MDD (PTSD−MDD−; N = 18). Participants with PTSD demonstrated decreased ratios of GABA to glutamine relative to healthy PTSD−MDD− controls but no single‐metabolite abnormalities. When comorbid MDD was considered, however, MDD but not PTSD diagnosis was significantly associated with increased mPFC glutamine concentration and decreased glutamate:glutamine ratio. In addition, all participants with PTSD and/or MDD collectively demonstrated decreased glutathione relative to healthy PTSD−MDD− controls. Despite limited findings in single metabolites, patterns of abnormality in prefrontal metabolite concentrations among individuals with PTSD and/or MDD enabled supervised classification to separate them from healthy controls with 80+% sensitivity and specificity, with glutathione, glutamine, and myoinositol consistently among the most informative metabolites for this classification. Our findings indicate that MDD can be an important factor in mPFC glutamate metabolism abnormalities observed using 1H MRS in cohorts with PTSD. [ABSTRACT FROM AUTHOR]

Alcohol use disorder (AUD) and chronic pain disorders are pervasive, multifaceted medical conditions that often co-occur. However, their comorbidity is often overlooked, despite its prevalence and clinical relevance. Individuals with AUD are more likely to experience chronic pain than the general population. Conversely, individuals with chronic pain commonly alleviate their pain with alcohol, which may escalate into AUD. This narrative review discusses the intricate relationship between AUD and chronic pain. Based on the literature available, the authors present a theoretical model explaining the reciprocal relationship between AUD and chronic pain across alcohol intoxication and withdrawal. They propose that the use of alcohol for analgesia rapidly gives way to acute tolerance, triggering the need for higher levels of alcohol consumption. Attempts at abstinence lead to alcohol withdrawal syndrome and hyperalgesia, increasing the risk of relapse. Chronic neurobiological changes lead to preoccupation with pain and cravings for alcohol, further entrenching both conditions. To stimulate research in this area, the authors review methodologies to improve the assessment of pain in AUD studies, including self-report and psychophysical methods. Further, they discuss pharmacotherapies and psychotherapies that may target both conditions, potentially improving both AUD and chronic pain outcomes simultaneously. Finally, the authors emphasize the need to manage both conditions concurrently, and encourage both the scientific community and clinicians to ensure that these intertwined conditions are not overlooked given their clinical significance. [ABSTRACT FROM AUTHOR]

Introduction Over the past decade, 12-month alcohol use, high-risk drinking, and alcohol use disorder (AUD) have increased by 11.2%, 29.9%, and 49.4%, respectively, in the United States. (1) In addition [...]

Background: Effective pharmacologic treatments for comorbid alcohol use disorder (AUD) and posttraumatic stress disorder (PTSD) are lacking. Kappa (κ) opioid receptor antagonists may address this unmet need. Buprenorphine is a κ‐opioid antagonist and a partial agonist of mu (μ) opioid receptors. Whereas naltrexone blocks all μ‐mediated effects combining it with buprenorphine yields a pharmacologic net effect of opioid receptor antagonism. Because no κ‐opioid receptor antagonist it available for clinical use, we tested this combination in a proof‐of‐concept study. Methods: Consenting participants were enrolled in a Phase II, multisite, double‐blind, randomized, placebo‐controlled trial evaluating the effectiveness of sublingual (SL) buprenorphine combined with extended‐release (XR) injectable naltrexone for the treatment of comorbid AUD and PTSD. Eligible participants (n = 75) were randomized (1:1:1) to receive either buprenorphine 2 mg/day plus naltrexone‐XR (n = 35), buprenorphine 8 mg/day plus naltrexone‐XR (n = 6) or SL plus injectable placebo (n = 34) for 12 weeks. The buprenorphine 8 mg/day plus naltrexone‐XR arm was dropped early in the trial due to the negative impact of COVID‐19 on enrollment. A binary primary outcome of response at week 8 was defined as a decrease from baseline of ≥10 points on the past week Clinician‐Administered PTSD Scale (CAPS‐5) and a reduction of ≥1 of past month alcohol risk level, as defined by the World Health Organization (WHO) and measured by the Timeline Follow‐Back. Results: Based on the results of a futility analysis, enrollment was stopped prior to reaching the initial goal of 90 participants. At the week eight primary timepoint, there were no statistically significant differences between buprenorphine plus naltrexone‐XR and placebo group for the primary composite outcome (OR = 0.63; p‐value = 0.52), or the subcomponents of the PTSD outcome (OR = 0.76; p‐value = 0.69) and AUD outcome (OR = 0.17; p‐value = 0.08). The placebo arm had a significantly higher proportion of participants with ≥1 WHO risk level reduction than the buprenorphine plus naltrexone‐XR arm (OR = 0.18, p value = 0.02). Conclusions: This is the first study to evaluate the potential of κ‐opioid receptor antagonism for the treatment of comorbid AUD and PTSD. The combination of buprenorphine and naltrexone‐XR showed no significant improvement over placebo for the composite, PTSD, or alcohol measures. [ABSTRACT FROM AUTHOR]

When a person consumes ethanol, the body quickly begins to convert it to acetic acid, which circulates in the blood and can serve as a source of energy for the [...]