A systematic review of oculomotor deficits associated with acute and chronic cannabis use.

Driving is a critical everyday task necessitating the rapid and seamless integration of dynamic visually derived information to guide neurobehaviour. Biological markers are frequently employed to detect Δ9-tetrahydrocannabinol (THC) consumption among drivers during roadside tests, despite not necessarily indicating impairment. Characterising THC-specific alterations to oculomotor behaviour may offer a more sensitive measure for indexing drug-related impairment, necessitating discrimination between acute THC effects, chronic use and potential tolerance effects. The present review aims to synthesise current evidence on the acute and chronic effects of THC on driving-relevant oculomotor behaviour. The review was prospectively registered (10.17605/OSF.IO/A4H9W), and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines informed reporting standards. Overall, 20 included articles comprising 12 experimental acute dosing trials, 5 cross-sectional chronic use studies and 3 roadside epidemiological studies examined the effects of cannabis/THC on oculomotor parameters including saccadic activity gaze behaviour, nystagmus, smooth pursuit and eyelid/blink characteristics. Acute THC consumption selectively impacts oculomotor control, notably increasing saccadic latency and inaccuracy and impairing inhibitory control. Chronic cannabis users, especially those with early age of use onset, display enduring oculomotor deficits that affect visual scanning efficiency. The presence of eyelid tremors appears to be a reliable indicator of cannabis consumption while remaining distinct from direct impairment associated with visual attention and motor control. Cannabis selectively influences oculomotor activity relevant to driving, highlighting the role of cannabinoid systems in these processes. Defining cannabis/THC-specific changes in oculomotor control may enhance the precision of roadside impairment assessments and vehicle safety systems to detect drug-related impairment and assess driving fitness.

Acute effects of amphetamine and related psychostimulants on impulsivity: a systematic review of clinical trials.

Evidence for acute amphetamine effects on behavioural impulsivity in healthy populations remains elusive and, at times, mixed. This review collates and reviews the clinical literature on the acute effects of amphetamines on measures of behavioural impulsivity in healthy adults. Randomised and placebo-controlled clinical trials that assessed behavioural impulsivity following the administration of an acute dose of amphetamine or a related psychostimulant (including amphetamine analogues and methylphenidate) were eligible for inclusion. The EBSCOHost, SCOPUS, PsychNet, Web of Science and ProQuest databases were searched from inception to 26 April 2021. Study selection, data extraction and the Cochrane risk of bias assessments were conducted by two independent reviewers. Reporting follows PRISMA guidelines, and the review was registered a priori on the PROSPERO database (Registration No: CRD42021249861). A total of 20 studies were included, comprising a total of 737 participants. Overall, results indicate that low-moderate doses of amphetamine and related psychostimulants may improve (i.e., reduce) impulsive responding without compromising performance, reflecting enhanced inhibitory control of behaviour. These effects are mild and appear most pronounced in individuals with high baseline impulsivity. This review highlights the need for greater consistency in behavioural task selection and future high-quality and well-designed studies to address current concerns around growing prescription psychostimulant use and misuse.

The prevalence of alcohol use and risky driving practises among individuals who consume sedatives nonmedically: findings from the NESARC-III.

Background: Worldwide, 1.3 million people die because of a road traffic collision each year, with over half (57.7%) of such deaths in the United States involving a psychoactive substance. The prevalence of drink-drivers is slowly declining; however, the number of drivers under the influence of other drugs, such as sedatives, continues to rise.Objectives: This study aimed to examine alcohol use and risky driving practices among individuals who consume sedatives nonmedically.Methods: A total of 36,309 US adults (48.1% male) who participated in wave 3 (2012) of the National Epidemiologic Survey on Alcohol and Related Conditions were included for analysis.Results: Overall, 827 respondents reported past-year nonmedical sedative use. Almost two-third (64.9%) of these individuals exceeded recommended drinking guidelines and 42.5% met the criteria for a past-year DSM-5 alcohol use disorder. When controlling for demographic, lifestyle, and health factors, they were 1.84 times as likely to drink-drive (95% confidence interval = 1.46-2.33, p < .001) compared to those not using sedatives or using them as prescribed. Among those who reported both drink-driving and driving under the influence of sedatives in the last 12 months, 68.1% met the criteria for a past-year DSM-5 sedative use disorder.Conclusion: Several driving outcomes relevant to road safety, such as driving under the influence of alcohol or sedatives, are impacted by sedative consumption. Given that individuals who consume sedatives nonmedically may be unaware or misperceive the impacts of substance use on safe driving, interventions to reduce such behavior should be targeted among this high-risk group.

Driving Simulator Performance After Administration of Analgesic Doses of Ketamine With Dexmedetomidine or Fentanyl.

PURPOSE/BACKGROUND: As a sole agent, ketamine acutely compromises driving ability; however, performance after coadministration with the adjuvant sedating agents dexmedetomidine or fentanyl is unclear. METHODS/PROCEDURES: Using a randomized within-subject design, 39 participants (mean ± SD age, 28.4 ± 5.8 years) received 0.3 mg/kg bolus followed by 0.15 mg kg h infusion of ketamine (3-hour duration), in addition to either (i) 0.7 µg kg h infusion of dexmedetomidine for 1.5 hours (n = 19; KET/DEX) or (ii) three 25 µg fentanyl injections for 1.5 hours (n = 20; KET/FENT). Whole blood drug concentrations were determined during ketamine only, at coadministration (KET/DEX or KET/FENT) and at 2 hours after treatment. Subjective effects were determined using a standardized visual analog scale. Driving performance was assessed at baseline and at posttreatment using a validated computerized driving simulator. Primary outcomes included SD of lateral position (SDLP) and steering variability (SV). FINDINGS/RESULTS: Administration of ketamine with dexmedetomidine but not fentanyl significantly increased SDLP (F1,18 = 22.60, P < 0.001) and reduced SV (F1,18 = 164.42, P < 0.001) 2 hours after treatment. These deficits were comparatively greater for the KET/DEX group than for the KET/FENT group (t37 = -5.21 [P < 0.001] and t37 = 5.22 [P < 0.001], (respectively). For the KET/DEX group, vehicle control (SV) and self-rated performance (visual analog scale), but not SDLP, was inversely associated with ketamine and norketamine blood concentrations (in nanograms per milliliter). Greater subjective effects were moderately associated with driving deficits. IMPLICATIONS/CONCLUSIONS: Driving simulator performance is significantly compromised after coadministration of analgesic range doses of ketamine with dexmedetomidine but not fentanyl. An extended period of supervised driver abstinence is recommended after treatment, with completion of additional assessments to evaluate home readiness.

When should the driver with a history of substance misuse be allowed to return to the wheel? A review of the substance misuse section of the Australian national guidelines.

Assessing fitness to drive in applicants with a historical or current substance use disorder presents a specific clinical challenge. The Australian guidelines require evidence of remission and absence of cognitive change when considering applications for re-licensing driver or individuals applying to reengage in safety-sensitive work. This paper reviews some of the clinical and biochemical indicators that determine whether a particular person is in 'remission' and meets the criteria for return to driving or other safety-sensitive occupation. It provides an overview of the challenges in establishing an evidence-based approach to determining fitness for safety critical activities. There is no internationally accepted definition of 'remission'. Review of the literature and examination of assessment protocols from other national jurisdictions are available for alcohol and the more important drugs of interest in road safety. Assessing fitness to drive when there is a history of substance misuse and/or substance use disorders is a complex issue that requires assessment of biomarkers, clinical findings and clinical assessment before the person returns to driving. We propose that hair testing provides a reliable and reproducible way to demonstrate remission and provide cost-effective monitoring. Standardised psychological tests could provide a reproducible assessment of the cognitive effects of drug use and suitability to resume driving. We recommend that AustRoads amend the national guidelines to reflect an evidence-based approach to assessing fitness to drive after conviction for offences related to alcohol and drug use.

The association between gastroesophageal reflux disease with sleep quality, depression, and anxiety in a cohort study of Australian men.

BACKGROUND AND AIM: Previous clinical studies have demonstrated a relationship between gastroesophageal reflux disease (GERD) with anxiety and depression; however, few population-based studies have controlled for sleep disorders. The current study aimed to assess the relationship between GERD and anxiety, depression, and sleep disorders in a community-based sample of Australian men. METHODS: Participants comprised a subset of 1612 men (mean age: 60.7 years, range: 35-80) who participated in the Men Androgen Inflammation Lifestyle Environment and Stress Study during the years 2001-2012, who had complete GERD measures (Gastresophageal Reflux Disease Questionnaire), and were not taking medications known to impact gastrointestinal function (excluding drugs taken for acid-related disorders). Current depression and anxiety were defined by (i) physician diagnosis, (ii) symptoms of depression (Beck Depression Inventory and Centre for Epidemiological Studies Depression Scale) or anxiety (Generalized Anxiety Disorder-7), and/or current depressive or anxiolytic medication use. Previous depression was indicated by past depressive diagnoses/medication use. Data on sleep quality, daytime sleepiness, and obstructive sleep apnea were collected along with several health, lifestyle, and medical factors, and these were systematically evaluated in both univariate and multivariable analyses. RESULTS: Overall, 13.7% (n = 221) men had clinically significant GERD symptoms. In the adjusted models, an association between GERD and anxiety (odds ratio [OR] 2.7; 95% confidence interval [CI] 1.0-6.8) and poor sleep quality (OR 1.8; 95% CI 1.2-2.9) was observed; however, no effect was observed for current depression (OR 1.5; 95% CI 0.8-2.7). After removing poor sleep quality from the model, an independent association between current depression (OR 2.6; 95% CI 1.7-3.8) and current anxiety (OR 3.2; 95% CI 1.8-6.0) and GERD was observed, but not for previous depression (OR 1.4; 95% CI 0.7-2.8). CONCLUSION: In this sample of urban-dwelling men, we observed a strong independent association between GERD, anxiety, and current depression, the latter appearing to be partly mediated by poor sleep quality. Patients presenting with GERD should have concurrent mental health assessments in order to identify potential confounders to the successful management of their symptoms.

Recreational stimulants, herbal, and spice cannabis: The core psychobiological processes that underlie their damaging effects.

AIMS: Recreational drugs are taken for their positive mood effects, yet their regular usage damages well-being. The psychobiological mechanisms underlying these damaging effects will be debated. METHODS: The empirical literature on recreational cannabinoids and stimulant drugs is reviewed. A theoretical explanation for how they cause similar types of damage is outlined. RESULTS: All psychoactive drugs cause moods and psychological states to fluctuate. The acute mood gains underlie their recreational usage, while the mood deficits on withdrawal explain their addictiveness. Cyclical mood changes are found with every central nervous system stimulant and also occur with cannabis. These mood state changes provide a surface index for more profound psychobiological fluctuations. Homeostatic balance is altered, with repetitive disturbances of the hypothalamic-pituitary-adrenal axis, and disrupted cortisol-neurohormonal secretions. Hence, these drugs cause increased stress, disturbed sleep, neurocognitive impairments, altered brain activity, and psychiatric vulnerability. Equivalent deficits occur with novel psychoactive stimulants such as mephedrone and artificial "spice" cannabinoids. These psychobiological fluctuations underlie drug dependency and make cessation difficult. Psychobiological stability and homeostatic balance are optimally restored by quitting psychoactive drugs. CONCLUSIONS: Recreational stimulants such as cocaine or MDMA (3.4-methylenedioxymethamphetamine) and sedative drugs such as cannabis damage human homeostasis and well-being through similar core psychobiological mechanisms.

DSM-5 Tobacco Use Disorder and Sleep Disturbance: Findings from the National Epidemiologic Survey on Alcohol and Related Conditions-III (NESARC-III).

INTRODUCTION: The DSM-5 Tobacco use disorder diagnosis incorporates tobacco misuse, addictive behaviors and withdrawal symptomology. Tobacco use is bidirectionally associated with sleep pathology; however, no epidemiological studies have yet evaluated the associations between DSM-5 Tobacco use disorder and self-reported sleep disturbance. The current study aimed to evaluate health, medical and sleep-related factors among individuals within this diagnostic stratum. METHOD: A total of N = 36,177 adults who participated in the 2012-2013 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC-III) were included for analyses. The adjusted odd ratios (AOR) for individual classifications of DSM-5 Tobacco use disorder among those with subjective sleep disturbances were used as the primary outcome measure and relevant demographic, clinical and medical factors were considered in all univariate and multivariable analyses. RESULTS: Current and lifetime DSM-5 tobacco use disorder diagnoses were associated with poorer health and medical outcomes and higher rates of subjective sleep disturbances (all p < 0.001). Associations between current and lifetime DSM-5 tobacco use disorder and subjective sleep disturbances were maintained in multivariable analyses following adjustment for a range of health, lifestyle, and psychiatric factors (adjusted OR 1.11, 95%CI 1.00-1.23 and adjusted OR = 1.24, 95%CI 1.15-1.34, respectively); however, these relationships were fully explained by diagnoses of DSM-5 alcohol use disorder. CONCLUSIONS: Data from this large, representative survey indicate that the association between DSM-5 Tobacco use disorder and sleep disturbance is explained by underlying diagnoses of DSM-5 alcohol use disorder. Multifaceted substance abuse treatment protocols may improve treatment outcomes for affected patient groups.

Social and emotional loneliness and self-reported difficulty initiating and maintaining sleep (DIMS) in a sample of Norwegian university students.

Social and emotional loneliness negatively impact several areas of health, including sleep. However, few comprehensive population-based studies have evaluated this relationship. Over 12,000 students aged 21-35 years who participated in the student survey for higher education in Norway (the SHoT study) were assessed. Loneliness was assessed using the Social and Emotional Loneliness Scale. Difficulty initiating and maintaining sleep (DIMS) was assessed by a single-item subjective response on the depression scale of the Hopkins Symptoms Checklist (HSCL-25). Social loneliness was associated with more serious DIMS (unadjusted proportional odds-ratio [OR] = 2.69, 95% CI = 2.46-2.95). This association was attenuated following adjustment for anxiety (adjusted OR = 1.92, 95% CI = 1.75-2.10) and depression (adjusted OR = 1.48, 95% CI = 1.34-1.63), however was not substantially altered when all demographics and psychological distress were accounted for (fully adjusted OR = 1.46, 95% CI = 1.30-1.63). Emotional loneliness was also associated with more serious DIMS (unadjusted proportional OR = 2.33, 95% CI = 2.12-2.57). Adjustment for anxiety (adjusted OR = 1.96, 95% CI = 1.78-2.15) and depression (adjusted OR = 1.64, 95% CI = 1.48-1.80) attenuated, but did not extinguish this relationship in the fully adjusted model (adjusted OR = 1.22, 95% CI = 1.09-1.31). Mediation analyses revealed that the social loneliness-DIMS association was fully attributed to psychological distress, while the emotional loneliness-DIMS association was only partially mediated, and a direct association was still observed. Associations between social and emotional loneliness and subjective DIMS were embedded in a larger pattern of psychological distress. Mitigating underlying feelings of loneliness may reduce potentially deleterious effects on sleep health and psychological wellbeing in young adults.

Trajectories and stability of self-reported short sleep duration from adolescence to adulthood.

The trajectories and stability of self-reported sleep duration recorded at ages 13, 15, and 23 years on reported sleep duration at age 30 years among 1105 students (55% male) who participated in the Norwegian Longitudinal Health and Behaviour Study were examined. Questionnaire data were used to obtain demographic and sleep variables. Dichotomised short sleep duration was based on normative values and set as ≤ 8.5 h (age 13 years), ≤ 8 h (age 15 years) and ≤ 7 h (ages 23 and 30 years). Results indicated a significant overall reduction in total sleep duration (h per night) across age groups. Sleep duration (continuous) at age 15 and 23 years (whole group) was moderately but positively correlated with sleep duration at age 30 years (P < 0.01). When split by sex, at age 15 years, this association was present among females only (P < 0.01); however, at age 23 years, this association was present in both male and females (both P < 0.001). Categorical short sleep at age 23 years (whole group) was associated with short sleep at age 30 years (unadjusted odds ratio = 3.67, 95% confidence interval 2.36-5.69). Following sex stratification, this effect was significant for both males (unadjusted odds ratio = 3.77, 95% confidence interval: 2.22-6.42) and females (unadjusted odds ratio = 2.71, 95% confidence interval: 1.46-5.04). No associations were noted for categorical short sleep at ages 13 or 15 years, and subsequent short sleep at 30 years. Habitual short sleep duration during middle adulthood is not sustained from the time of early adolescence. Rather, these trends appear to be formed during early adulthood.

Excessive daytime sleepiness and falls among older men and women: cross-sectional examination of a population-based sample.

BACKGROUND: Excessive daytime sleepiness (EDS) has been associated with an increased risk for falls among clinical samples of older adults. However, there is little detailed information among population-representative samples. The current study aimed to assess the relationship between EDS and falls among a cohort of population-based older adults. METHODS: This study assessed 367 women aged 60-93 years (median 72, interquartile range 65-79) and 451 men aged 60-92 years (median 73, interquartile range 66-80) who participated in the Geelong Osteoporosis Study between the years 2001 and 2008. Falls during the prior year were documented via self-report, and for men, falls risk score was obtained using an Elderly Fall Screening Test (EFST). Sleepiness was assessed using the Epworth Sleepiness Scale (ESS), and scores of ≥ 10 indicated EDS. Differences among those with and without EDS in regard to falls were tested using logistic regression models. RESULTS: Among women, 50 (13.6%) individuals reported EDS. Women with EDS were more likely to report a fall, and were more likely to report the fall occurring outside. EDS was similarly associated with an increased risk of a fall following adjustment for use of a walking aid, cases of nocturia and antidepressant medication use (adjusted OR = 2.54, 95% CI 1.24-5.21). Multivariate modelling revealed antidepressant use (current) as an effect modifier (p < .001 for the interaction term). After stratifying the data by antidepressant medication use, the association between EDS and falls was sustained following adjustment for nocturia among antidepressant non-users (adjusted OR = 2.63, 95% CI 1.31-5.30). Among men, 72 (16.0%) individuals reported EDS. No differences were detected for men with and without EDS in regard to reported falls, and a trend towards significance was noted between EDS and a high falls risk as assessed by the EFST (p = 0.06), however, age explained this relationship (age adjusted OR = 2.20, 95% CI 1.03-1.10). CONCLUSIONS: For women, EDS is independently associated with at least one fall during the previous year, and this is more likely to occur whilst located outside. Amelioration of EDS may assist in improving functional outcomes among these individuals by reducing the risk for falls.

The relationships between insomnia, sleep apnoea and depression: findings from the American National Health and Nutrition Examination Survey, 2005-2008.

OBJECTIVE: To determine the association between insomnia, obstructive sleep apnoea (OSA), and comorbid insomnia-OSA and depression, while controlling for relevant lifestyle and health factors, among a large population-based sample of US adults. METHOD: We examined a sample of 11,329 adults (≥18 years) who participated in the National Health and Nutrition Examination Survey (NHANES) during the years 2005-2008. Insomnia was classified via a combination of self-reported positive physician diagnosis and high-frequency 'trouble falling asleep', 'waking during the night', 'waking too early', and 'feeling unrested during the day'. OSA was classified as a combination of a positive response to a physician-diagnosed condition, in addition to a high frequency of self-reported nocturnal 'snoring', 'snorting/stopping breathing' and 'feeling overly sleepy during the day'. Comorbid insomnia-OSA was further assessed by combining a positive response to either insomnia (all), or sleep apnoea (all), as classified above. Depressive symptomology was assessed by the Patient Health Questionnaire-9 (PHQ-9), with scores of >9 used to indicate depression. Odds ratios (ORs) and 95% confidence intervals (CIs) for sleep disorders and depression were attained from logistic regression modelling adjusted for sex, age, poverty level, smoking status and body mass index (BMI). RESULTS: Those who reported insomnia, OSA or comorbid insomnia-OSA symptoms reported higher rates of depression (33.6%, 22.2%, 27.1%, respectively), and consistently reported poorer physical health outcomes than those who did not report sleep disorders. After adjusting for sex, age, poverty level, smoking status and BMI (kg/m(2)), insomnia (OR 6.57, 95% CI 3.89-11.11), OSA (OR 5.14, 95% CI 3.14-8.41) and comorbid insomnia-OSA (OR 6.67, 95% CI 4.44-10.00) were associated with an increased likelihood of reporting depression. CONCLUSIONS: Insomnia, OSA and comorbid insomnia-OSA are associated with significant depressive symptomology among this large population-based sample of adults.

A randomised, placebo-controlled, double blind, crossover trial on the effect of a 20:1 cannabidiol: Δ9-tetrahydrocannabinol medical cannabis product on neurocognition, attention, and mood.

As cannabinoid-based medications gain popularity in the treatment of refractory medical conditions, it is crucial to examine the neurocognitive effects of commonly prescribed products to ensure associated safety profiles. The present study aims to investigate the acute effects of a standard 1 mL sublingual dose of CannEpil®, a medicinal cannabis oil containing 100 mg cannabidiol (CBD) and 5 mg Δ9-tetrahydrocannabinol (THC) on neurocognition, attention, and mood. A randomised, double-blind, placebo-controlled, within-subjects design assessed 31 healthy participants (16 female, 15 male), aged between 21 and 58 years, over a two-week experimental protocol. Neurocognitive performance outcomes were assessed using the Cambridge Neuropsychological Test Automated Battery, with the Profile of Mood States questionnaire, and the Bond-Lader Visual Analogue Scale used to assess subjective state and mood. CannEpil increased Total Errors in Spatial Span and Correct Latency (median) in Pattern Recognition Memory, while also increasing Efficiency Score (lower score indicates greater efficiency) relative to placebo (all p < .05). Subjective Contentedness (p < .01) and Amicability (p < .05) were also increased at around 2.5 h post dosing, relative to placebo. Drowsiness or sedative effect was reported by 23 % of participants between three to six hours post CannEpil administration. Plasma concentrations of CBD, THC, and their metabolites were not significantly correlated with any observed alterations in neurocognition, subjective state, or adverse event occurrence. An acute dose of CannEpil impairs select aspects of visuospatial working memory and delayed pattern recognition, while largely preserving mood states among healthy individuals. Intermittent reports of drowsiness and sedation underscore the inter-individual variability of medicinal cannabis effects on subjective state. (ANZCTR; ACTRN12619000932167; https://www.anzctr.org.au).

A semi-naturalistic open-label study examining the effect of prescribed medical cannabis use on simulated driving performance.

BACKGROUND: Despite increasing medical cannabis use, research has yet to establish whether and to what extent products containing delta-9-tetrahydrocannabinol (THC) impact driving performance among patients. Stable doses of prescribed cannabinoid products during long-term treatment may alleviate clinical symptoms affecting cognitive and psychomotor performance. AIM: To examine the effects of open-label prescribed medical cannabis use on simulated driving performance among patients. METHODS: In a semi-naturalistic laboratory study, 40 adults (55% male) aged between 23 and 80 years, consumed their own prescribed medical cannabis product. Driving performance outcomes including standard deviation of lateral position (SDLP), the standard deviation of speed (SDS), mean speed and steering variability were evaluated using the Forum8 driving simulator at baseline (pre-dosing), 2.5 h and 5 -h (post-dosing). Perceived driving effort (PDE) was self-reported after each drive. Oral fluid and whole blood samples were collected at multiple timepoints and analysed for THC via liquid chromatography-mass spectrometry. RESULTS: A significant main effect of time was observed for mean speed (p = 0.014) and PDE (p = 0.020), with patients displaying modest stabilisation of vehicle control, increased adherence to speed limits and reductions in PDE post-dosing, relative to baseline. SDLP (p = 0.015) and PDE (p = 0.043) were elevated for those who consumed oil relative to flower-based products. Detectable THC concentrations were observed in oral fluid at 6-h post-dosing (range = 0-24 ng/mL). CONCLUSIONS: This semi-naturalistic study suggests that the consumption of medical cannabis containing THC (1.13-39.18 mg/dose) has a negligible impact on driving performance when used as prescribed.

Trait anger as a predictor of dangerous driving behaviour amongst people who use methamphetamine.

INTRODUCTION: Despite increased prevalence of methamphetamine in road trauma, it remains unclear how its use translates to an increased risk of traffic-related harm. Exploration of psychosocial factors may thus help identify relevant predictors of dangerous driving behaviour among people who regularly consume methamphetamine. METHODS: Licenced individuals who report predominant and sustained methamphetamine use (at least 1-time/month for 6 months at heaviest use) were recruited from the Australian community and via targeted campaign (Eastern Health). Psychosocial, substance use and driving behaviour data (Dula Dangerous Driving Index, DDDI) were collected via a secure anonymous online forced-entry survey platform (Qualtrics). RESULTS: Seventy-seven individuals (65.5 % male) aged between 20-50 years [mean = 29.7, ± Standard Deviation (SD) 6.1] were included. Most (90 %) respondents met criteria for problematic methamphetamine use [Severity of Dependency Scale (SDS) score ≥ 5], and 75 % were high-risk alcohol consumers [Alcohol Use Disorders Identification Test (AUDIT-C) score ≥ 4 for men and ≥ 3 for women]. On average, age of first methamphetamine use occurred at 23.3 years (±5.2). A best-possible subset's regression selection method with dangerous driving behaviour as the dependent variable determined the model with three predictors (alcohol use, substance dependence severity and trait anger) as most parsimonious. After controlling for substance use, trait anger strongly and positively predicted dangerous driving behaviour as measured by the DDDI ([F(3,74) = 26.06, p < .001, adjusted R2 = 0.50, Cohens f2 = 0.42). DISCUSSION AND CONCLUSIONS: Trait anger is a strong predictor of risky driving among road users who use methamphetamine. Interactions between stable negative-emotional and situational traffic and driving-related factors may increase risk of harm through greater engagement in risk-taking behaviour.

Cannabidiol for moderate-severe insomnia: a randomized controlled pilot trial of 150 mg of nightly dosing.

STUDY OBJECTIVES: Low-dose cannabidiol (CBD) has become readily available in numerous countries; however, little consensus exists on its efficacy as a sleep aid. This trial explored the efficacy of 150 mg of CBD (n = 15) compared with placebo (n = 15) as a sleep aid in primary insomnia. CBD supplementation was hypothesized to decrease insomnia symptoms and improve aspects of psychological health, relative to placebo. METHODS: Using a randomized, placebo-controlled, parallel design featuring a single-blind placebo run-in week followed by a 2-week double-blind randomized dosing phase, participants consumed the assigned treatment sublingually 60 minutes before bed nightly. Wrist-actigraphy and sleep diaries measured daily sleep. Sleep quality, sleep effort, and well-being were measured weekly over 4 in-laboratory visits. Insomnia severity and trait anxiety were measured at screening and study conclusion. RESULTS: Insomnia severity, self-reported sleep-onset latency, sleep efficiency, and wake after sleep onset did not differ between treatments throughout the trial (all P > .05). Compared with placebo, the CBD group reported greater well-being scores throughout the trial (trial end mean difference = 2.60; standard error: 1.20), transient elevated behavior following wakefulness scores after 1 week of treatment (mean difference = 3.93; standard error: 1.53), and had superior objective sleep efficiency after 2 weeks of treatment (mean difference = 6.85; standard error: 2.95) (all P < .05). No other significant treatment effects were observed. CONCLUSIONS: Nightly supplementation of 150 mg CBD was similar to placebo regarding most sleep outcomes while sustaining greater well-being, suggesting more prominent psychological effects. Additional controlled trials examining varying treatment periods and doses are crucial. CLINICAL TRIAL REGISTRATION: Registry: Australian New Zealand Clinical Trials Registry; Name: Cannabidiol (CBD) treatment for insomnia; URL: https://anzctr.org.au/Trial/Registration/TrialReview.aspx?ACTRN=12620000070932; Identifier: ACTRN12620000070932. CITATION: Narayan AJ, Downey LA, Rose S, Di Natale L, Hayley AC. Cannabidiol for moderate-severe insomnia: a randomized controlled pilot trial of 150 mg of nightly dosing. J Clin Sleep Med. 2024;20(5):753-763.

So depression is an inflammatory disease, but where does the inflammation come from?

BACKGROUND: We now know that depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, as well as activation of the compensatory anti-inflammatory reflex system. It is similarly accompanied by increased oxidative and nitrosative stress (O&NS), which contribute to neuroprogression in the disorder. The obvious question this poses is 'what is the source of this chronic low-grade inflammation?' DISCUSSION: This review explores the role of inflammation and oxidative and nitrosative stress as possible mediators of known environmental risk factors in depression, and discusses potential implications of these findings. A range of factors appear to increase the risk for the development of depression, and seem to be associated with systemic inflammation; these include psychosocial stressors, poor diet, physical inactivity, obesity, smoking, altered gut permeability, atopy, dental cares, sleep and vitamin D deficiency. SUMMARY: The identification of known sources of inflammation provides support for inflammation as a mediating pathway to both risk and neuroprogression in depression. Critically, most of these factors are plastic, and potentially amenable to therapeutic and preventative interventions. Most, but not all, of the above mentioned sources of inflammation may play a role in other psychiatric disorders, such as bipolar disorder, schizophrenia, autism and post-traumatic stress disorder.

The relationship between excessive daytime sleepiness and depressive and anxiety disorders in women.

OBJECTIVE: Excessive daytime sleepiness (EDS) is a common clinical symptom that affects women more than men. However, the association of excessive sleepiness with depressive and anxiety disorders in the broader population is unclear. The aim of this study was, therefore, to examine the association between excessive daytime sleepiness as measured by the Epworth Sleepiness Scale, and depressive and anxiety disorders in a population-based sample of women. METHODS: Using the Structured Clinical Interview for DSM-IV Disorders (Non-Patient) (SCID-I/NP), 944 women aged 20-97 years (median 49 years, IQR 33-65 years) were assessed for depressive and anxiety disorders as part of the Geelong Osteoporosis Study. EDS was assessed using the Epworth Sleepiness Scale (ESS, cut-off > 10). Lifestyle factors were documented by self-report, height and weight were measured, and socioeconomic status categorised according to the Index of Relative Socio-Economic Advantage and Disadvantage. RESULTS: Overall, 125 (13.2%) of the women were identified with EDS. EDS was associated with an increased likelihood for both current (OR = 2.11, 95% CI 1.10-4.06) and lifetime history (OR = 1.95, 95% CI 1.28-2.97) of depressive disorders, but not anxiety disorders, independent of age and alcohol consumption. These findings were not explained by antidepressant or sedative use, body mass index, physical activity, smoking, or socioeconomic status. CONCLUSIONS: These results suggest that excessive daytime sleepiness is associated with current and lifetime depressive, but not anxiety disorders. Clinically, this highlights the need to take into account the possible bidirectional relationship between depressive disorders and excessive sleepiness when assessing mental health issues in patients with EDS.