Anxiety disorders are the most common mental diseases. Anxiety and the associated physical symptoms may disturb social and occupational life and increase the risk of somatic diseases. The pathophysiology of anxiety development is complex and involves alterations in stress hormone production, neurosignaling pathways or free radical production. The various manifestations of anxiety, its complex pathophysiological background and the side effects of available treatments underlie the quest for constantly seeking therapies for these conditions. Melatonin, an indolamine produced in the pineal gland and released into the blood on a nightly basis, has been demonstrated to exert anxiolytic action in animal experiments and different clinical conditions. This hormone influences a number of physiological actions either via specific melatonin receptors or by receptor-independent pleiotropic effects. The underlying pathomechanism of melatonin’s benefit in anxiety may reside in its sympatholytic action, interaction with the renin–angiotensin and glucocorticoid systems, modulation of interneuronal signaling and its extraordinary antioxidant and radical scavenging nature. Of importance, the concentration of this indolamine is significantly higher in cerebrospinal fluid than in the blood. Thus, ensuring sufficient melatonin production by reducing light pollution, which suppresses melatonin levels, may represent an endogenous neuroprotective and anxiolytic treatment. Since melatonin is freely available, economically undemanding and has limited side effects, it may be considered an additional or alternative treatment for various conditions associated with anxiety.

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Melatonin as a Potential Approach to Anxiety Treatment

Alzheimer’s disease (AD) is a leading neurodegenerative condition causing cognitive and memory decline. With small-molecule drugs targeting Aβ proving ineffective, alternative targets are urgently needed. Neuroinflammation, which is central to AD’s pathology, results in synaptic and neuronal damage, highlighting the importance of addressing inflammation and conserving neuronal integrity. Cannabidiol (CBD), derived from cannabis, is noted for its neuroprotective and anti-inflammatory properties, having shown efficacy in neuropathic pain management for epilepsy. To investigate the therapeutic efficacy of CBD in AD and to elucidate its underlying mechanisms, we aimed to contribute valuable insights for incorporating AD prevention recommendations into future CBD nutritional guidelines. Aβ1–42 was employed for in vivo or in vitro model establishment, CBD treatment was utilized to assess the therapeutic efficacy of CBD, and RNA-seq analysis was conducted to elucidate the underlying therapeutic mechanism. CBD mitigates Aβ-induced cognitive deficits by modulating microglial activity, promoting neurotrophic factor release, and regulating inflammatory genes. The administration of CBD demonstrated a protective effect against Aβ toxicity both in vitro and in vivo, along with an amelioration of cognitive impairment in mice. These findings support the potential inclusion of CBD in future nutritional guidelines for Alzheimer’s disease prevention.

Assessing Cannabidiol as a Therapeutic Agent for Preventing and Alleviating Alzheimer’s Disease Neurodegeneration

The role of central neurotransmitters in appetite regulation of broilers and layers: similarities and differences

Cannabidiol (CBD), a cannabinoid that does not create psychoactive activities, has been identified as having a multitude of therapeutic benefits. This study delves into the chemical properties, pharmacokinetics, safety and toxicity, pharmacological effects, and most importantly, the association between the therapeutic potential of CBD and the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. The relationship between Nrf2 and CBD is closely linked to certain proteins that are associated with cardiovascular dysfunctions, cancers, and neurodegenerative conditions. Specifically, Nrf2 is connected to the initiation and progression of diverse health issues, including nephrotoxicity, bladder-related diseases, oral mucositis, cancers, obesity, myocardial injury and angiogenesis, skin-related inflammations, psychotic disorders, neuropathic pain, Huntington's disease, Alzheimer's disease, Parkinson's disease, neuroinflammation, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis. The association between CBD and Nrf2 is a zone of great interest in the medical field, as it has the potential to significantly impact the treatment and prevention of wide-ranging health conditions. Additional investigation is necessary to entirely apprehend the mechanisms underlying this crucial interplay and to develop effective therapeutic interventions. 

Therapeutic potentials of cannabidiol: Focus on the Nrf2 signaling pathway

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 to 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 two-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 four in-lab visits. Insomnia severity and trait anxiety were measured at screening and study conclusion.


RESULTS
Insomnia severity, subjective sleep onset latency, sleep efficiency and wake after sleep onset did not differ between treatments throughout the trial (all p>0.05). Compared to placebo, the CBD group reported greater well-being scores throughout the trial (trial end mean difference=2.60, SE 1.20), transient elevated behavior following wakefulness scores after 1 week of treatment (mean difference=3.93, SE 1.53) and had superior objective sleep efficiency after 2 weeks of treatment (mean difference=6.85, SE 2.95) (all p<0.05). No other significant treatment effects were observed.


CONCLUSIONS
Nightly supplementation of 150 mg CBD was similar to placebo regarding most sleep outcomes whilst 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; Title: Cannabidiol (CBD) treatment for insomnia; Identifier: ACTRN12620000070932; URL: https://anzctr.org.au/Trial/Registration/TrialReview.aspx?ACTRN=12620000070932.

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

Cannabinoid treatments for anxiety: A systematic review and consideration of the impact of sleep disturbance

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.

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

Abstract Introduction Cannabidiol (CBD) may have sleep promoting effects, but clinical dosage and safety recommendations are still lacking. This study was the first to examine whether the approved Therapeutic Goods Association (TGA) daily over-the-counter maximum dose of oral CBD oil (150mg) improved the self-rated severity of primary insomnia and explored CBD effects on higher-order cognitive performance tasks. Methods Participants (n = 30) with moderate-severe primary insomnia completed a one-week single-blind placebo-run in period followed by a 2-week double blind, parallel, randomised placebo-controlled dosing period with four assessment visits (V0-V4). Intra-group and between-group Insomnia Severity Index (ISI) (V0 and V4) and cognitive performance (ECog Pro) (V1, V2 and V4) outcomes were assessed using paired sample t-test with independent t-tests, and separate linear mixed effect models with Maximum Likelihood Estimation and independent T-tests, respectively. Results Preliminary findings showed reduced ISI for treatment (n = 5; baseline mean 16.60 to 9.60 post treatment, mean difference = -7.00, SD = 4.47) and placebo (n = 8; baseline mean 18.13 to 9.25 post treatment, mean difference = -8.88, SD = 3.68) over time (both p < .001). At conclusion, CBD did not outperform a placebo (p = .427). Numeric and spatial working memory accuracy (%) and reaction time (ms) indicated no intra-group or between-group differences at any time point (all p > 0.05). Discussion Decreased insomnia severity from moderate to subthreshold levels indicate potential clinical benefits of daily CBD supplementation as a sleep aid for primary insomnia. Preserved higher-order neurocognitive abilities suggest a good safety profile.

/pdf/o049-insomnia-severity-and-cognitive-performance-following-1o2vffim.pdf

O049 Insomnia severity and cognitive performance following two weeks’ nightly supplementation with 150mg Cannabidiol (CBD) for primary insomnia

Cannabinoid treatments are commonly used for sleep conditions, but the direct sedating effects of daytime treatment consumption and indirect effects on night-time sleep are unclear. This study measures the direct effects of low-dose cannabinoid treatments on daytime sleepiness and potential indirect night-time sleep effects in healthy adult, novice cannabis users. Using a double-blind, randomised, placebo-controlled cross-over design, participants were orally administered a standardised dose of 1 mL oil containing THC:CBD ratios of either 1:1, 1:16 or a placebo over five weekly in-lab visits. Daytime sleepiness was measured at 40, 135 and 265 min post-dosing using the Karolinska Sleepiness Scale (KSS). Indirect night-time sleep effects on total sleep time (TST), sleep-onset latency (SOL), and number of awakenings after onset were measured using daily wrist-actigraphy and sleep-diary entries during the 7-day washout period between treatments. Final analyses (N = 20) showed subjective sleepiness (KSS score) significantly increased (mean difference = 1.9, SE 0.25) from 40 min to 265 min post-treatment (p < 0.001). No significant differences were observed between treatments for KSS. Indirect sleep measures (TST, SOL, number of awakenings) showed no differences between treatments or over time (all p > 0.05). Daytime consumption of low-dose cannabinoid oils did not induce direct sleepiness or indirect night-time effects post-dosing among adults. Future studies would benefit from exploring pharmacokinetics and the possibility of treatment amplification of daytime fatigue, mood and cognitive changes to assist the development of therapeutic guidelines for safe daytime medical cannabis use. ACTRN12622001539729, 13 December 2022, prospectively registered.

Same-Day Sedative and Night-Time Sleep Effects Following Combined Cannabinoid Formulations: A Randomised-Controlled Trial

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