The adverse health and psychological consequences of cannabis dependence

People who become dependent on cannabis are more likely than infrequent users to experience any of the adverse health effects that are caused by chronic cannabis use. Dependent cannabis use is rare in comparison with the more prevalent pattern of experimental and intermittent use (Bachman et al., 1997), but it may nonetheless affect as many as 1% of adults in the USA and Australia in any 1 year (Anthony et al., 1994; Hall et al., 1999a). Dependent cannabis users typically smoke two or more cannabis cigarettes a day over periods of years or decades in a minority of cases (Copeland et al., 2001; Solowij, 2002; Swift et al., 1998b). This chapter summarizes the most probable adverse health effects that cannabis-dependent persons are at increased risk of experiencing. With few exceptions (e.g., Solowij et al., 2002; Taylor et al., 2000), the literature does not directly assess the adverse health effects of cannabis dependence. The most probable effects can nonetheless be inferred from the more common studies of the effects of long-term daily cannabis use because many daily users are dependent on cannabis (Swift et al., 1998a, 2001). The chapter reviews evidence on the adverse health effects of more or less daily use over periods of years during young adulthood, and among those who seek treatment in their mid-thirties who have used cannabis more or less daily for the past 15–20 years

The Endocannabinoid System and Cannabidiol's Promise for the Treatment of Substance Use Disorder

Substance use disorder is characterized by repeated use of a substance, leading to clinically significant distress, making it a serious public health concern. The endocannabinoid system plays an important role in common neurobiological processes underlying substance use disorder, in particular by mediating the rewarding and motivational effects of substances and substance-related cues. In turn, a number of cannabinoid drugs (e.g., rimonabant, nabiximols) have been suggested for potential pharmacological treatment for substance dependence. Recently, cannabidiol (CBD), a non-psychoactive phytocannabinoid found in the cannabis plant, has also been proposed as a potentially effective treatment for the management of substance use disorder. Animal and human studies suggest that these cannabinoids have the potential to reduce craving and relapse in abstinent substance users, by impairing reconsolidation of drug-reward memory, salience of drug cues, and inhibiting the reward-facilitating effect of drugs. Such functions likely arise through the targeting of the endocannabinoid and serotonergic systems, although the exact mechanism is yet to be elucidated. This article seeks to review the role of the endocannabinoid system in substance use disorder and the proposed pharmacological action supporting cannabinoid drugs' therapeutic potential in addictions, with a focus on CBD. Subsequently, this article will evaluate the underlying evidence for CBD as a potential treatment for substance use disorder, across a range of substances including nicotine, alcohol, psychostimulants, opioids, and cannabis. While early research supports CBD's promise, further investigation and validation of CBD's efficacy, across preclinical and clinical trials will be necessary

Effect of cannabidiol on cognition in a maternal immune activation (poly IC) model of schizophrenia

Abstract of a poster presentation

The Neurobiology of Cannabis Use Disorders: A Call for Evidence

Using cannabis is perceived by many as relatively harmless, but the adverse effects of problematic cannabis use are significant. Thirteen million individuals globally have Cannabis Use Disorders (CUDs; UNODC, 2015), with relapse rates comparable to those of other substance use disorders (~52–70%; Budney et al., 1999; Chauchard et al., 2013). Contrasting non-problematic recreational cannabis use, severe forms of CUD involve compulsive use despite significant harms to mental health; high stress levels (craving, withdrawal); cognitive deficits; academic and work absenteeism; and significant risky behaviors, such as driving and operating machinery while intoxicated. Worryingly, the concentration of Δ9-tetrahydrocannabinol, the compound driving the addiction liability of cannabis, has risen in cannabis products over the past decade (UNODC, 2015)

Cannabis-related hippocampal volumetric abnormalities specific to subregions in dependent users

Rationale - Cannabis use is associated with neuroanatomical alterations in the hippocampus. While the hippocampus is composed of multiple subregions, their differential vulnerability to cannabis dependence remains unknown. Objectives - The objective of the study is to investigate gray matter alteration in each of the hippocampal subregions (presubiculum, subiculum, cornu ammonis (CA) subfields CA1-4, and dentate gyrus (DG)) as associated with cannabis use and dependence. Methods - A total of 35 healthy controls (HC), 22 non-dependent (CB-nondep), and 39 dependent (CB-dep) cannabis users were recruited. We investigated group differences in hippocampal subregion volumes between HC, CB-nondep, and CB-dep users. We further explored the association between CB use variables (age of onset of regular use, monthly use, lifetime use) and hippocampal subregions in CB-nondep and CB-dep users separately. Results - The CA1, CA2/3, CA4/DG, as well as total hippocampal gray matter were reduced in volume in CB-dep but not in CB-nondep users, relative to HC. The right CA2/3 and CA4/DG volumes were also negatively associated with lifetime cannabis use in CB-dep users. Conclusions - Our results suggest a regionally and dependence-specific influence of cannabis use on the hippocampus. Hippocampal alteration in cannabis users was specific to the CA and DG regions and confined to dependent users

Familial analysis of MMN in cannabis users: A case study

Abstract presented at the 23rd Australasian Society for Psychophysiology Conference, 20-22 Nov 2013, Wollongong, Australi

An investigation of mismatch negativity in current and ex-cannabis users using a feature controlled method

Abstract presented at the 23rd Australasian Society for Psychophysiology Conference, 20-22 Nov 2013, Wollongong, Australi

Electrophysiological correlates of the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism

The brain-derived neurotrophic factor (BDNF) protein is essential for neuronal development. Val66Met (rs6265) is a functional polymorphism at codon 66 of the BDNF gene that affects neuroplasticity and has been associated with cognition, brain structure and function. The aim of this study was to clarify the relationship between BDNF Val66Met polymorphism and neuronal oscillatory activity, using the electroencephalogram (EEG), in a normative cohort. Neurotypical (N = 92) young adults were genotyped for the BDNF Val66Met polymorphism and had eyes open resting-state EEG recorded for four minutes. Focal increases in right fronto-parietal delta, and decreases in alpha-1 and right hemispheric alpha-2 amplitudes were observed for the Met/Met genotype group compared to Val/Val and Val/Met groups. Stronger frontal topographies were demonstrated for beta-1 and beta-2 in the Val/Met group versus the Val/Val group. Findings highlight BDNF Val66Met genotypic differences in EEG spectral amplitudes, with increased cortical excitability implications for Met allele carriers