In most users, inhalation or injection of modest amounts of cannabis increases sociability, relaxation and creativity. These mood enhancing and anxiolytic properties are the main incentives of the usage of marijuana. However, in contrast, a smaller grousmoking-weed1.jpgp of individuals, particularly first time users, experience a number of undesirable emotional effects after cannabis consumption, such as panic, phobic manifestations and dysphoria (Lee, Strote, & Wechsler, 2000; as cited in: Bortolato, Bini, & Tambaro, 2010).

In addition, cannabis has been documented to induce psychotic symptoms such as derealization, depersonalization, paranoia and auditory hallucinations. These alterations are commonly categorized in two different entities: toxic psychosis and functional psychosis. Toxic psychosis features euphoria, perceptual distortions, clouding of consciousness and cognitive deficits. On the other hand, functional psychosis is characterized by positive symptoms similar to those featured in schizophrenia, including bizarre and paranoid ideation, but there is no cognitive impairment. These disturbances are highly sensitive to antipsychotic agents and are documented to reflect an underlying disorder in predisposed individuals (Haas, Weiden, Sweeney, & Frances, 1991; as cited in: Bortolato et al., 2010)

One of the key factors that has been shown to influence the differential responsiveness to cannabis is the dose of exposure. In particular, in first time or non habitual users, low dosages of THC or marijuana are generally conducive to euphoria, hilarity, relaxation and subtle perceptual changes. However, higher concentrations are known to elicit fear, agitation and psychotic manifestations as well as attentional impairment (Slade, 2005; as cited in: Bortolato et al., 2010)

Prolonged consumption of cannabis, particularly in adolescence, is generally conducive to persistent affective and cognitive after-effects in adulthood. These alterations include avolition and alexithymia, as well as impairments in informational processing, sustained and distributed attention, spatial working memory, verbal fluency, decision making and executive abnormalities in cortical and hippocampal metabolism (Haas, Weiden, Sweeney,& Frances, 1991; as cited in: Bortolato et al., 2010).

Anxiety-Spectrum and Mood Disorders

Cannabis abuse and dependence are frequently combined with affective and anxiety disorders though very few studies have been focused on the pathophysiological link between these entities. While cannabis does not appear to play a conclusive role in affective and anxiety disorders, lines of evidence show that its consumption can profoundly affect the severity and the clinical presentation of their symptoms (Hajois & Freund, 2002; as cited in: Bortolato et al., 2010). A 3577115_f520.jpgnumber of studies have reported that this substance can precipitate the symptoms of anxiety, bipolar and depressive disorders and reduce the therapeutic efficacy of benchmark agents. However, several patients suffering from anxiety and mood disorders use cannabis as a relaxant and for self-therapeutic purposes. However, it is important to note that while the initial consumption of cannabis can have relaxant effects in patients suffering from anxiety, its chronic use can actually exacerbate the symptoms of these illnesses by dampening the functions of the endocannabinoid system (Hajois & Freund, 2002; as cited in: Bortolato et al., 2010)

*The endocannabinoid system refers to a group of neuromodulatory lipids and their receptors that are involved in a variety of physiological processes including appetite, pain sensation, mood, and memory.

Vulnerability Factors

The inter-individual effects and differences in the psychological and behavioural effects of cannabis are likely influenced by the interaction of additional vulnerability factors as well. These include but are not limited to: frequency and duration of use, dose consumed, and relative concentrations of ingredients. Vulnerability factors also play a predominant role both in terms of intrinsic factors (including genetic vulnerability, age, gender, and premorbid personality traits) and extrinsic factors (including exposure to stress and concomitant use of other drugs) (Syudo, Ando, & Minami, 2008; as cited in: Bortolato et al., 2010).


Adolescence has been shown to be an important vulnerability factor for cannabis-induced after-effects. Juvenile age plays a key role in the development of attentional alterations following acute cannabis use, which are not commonly observed in adult users. The impairments in sustained attention in chronic adult uses have been shown to increase in severity for users that initiated cannabis consumption before 15 years of age (Syudo, Ando, & Minami, 2008; as cited in: Bortolato et al, 2010). Early onset of cannabis consumption has been associated with a higher susceptibility to psychosis. It is then likely that early consumption of cannabis may interfere with critical neurodevelopmental processes occurring throughout adolescence, including synaptic sprouting and pruning, myelination and changes in neurotransmitter concentrations. The consequences of exposure to cannabis in such a critical and sensitive period of growing may be particularly severe if associated with factors such as genetic or environmental determinants and lead to profound alterations of specific mental health disorders (Syudo, Ando, & Minami, 2008; as cited in: Bortolato et al, 2010).


Some lines of clinical investigation have documented the existence of gender differences in the vulnerability to cannabhis-mediated changes, with a higher severity of anxiety- like manifestations in females (Syudo, Ando, & Minami, 2008; as cited in: Bortolato et al., 2010).

Environmental Contingencies

Stressful environmental situations are known to exacerbate the anxiety and aversive reactions associated with acute administration of cannabis. Early stress, particularly from child abuse or neglect, has been shown to interact with cannabis use as well (Syudo, Ando, & Minami, 2008; as cited in: Bortolato et al., 2010).
Hajois & Freund, 2002; as cited in: Bortolato et al., 2010