Studies show significant negative effects of smoking marijuana on physical and mental health as well as social and occupational functioning (Gazdek, 2014). Smoking marijuana is known to have hemodynamic consequences (Mittleman et al., 2001). Cannabis also has immunosuppressant and endocrine effects although the clinical significance of these is still not clear (Ashton, 2001). Cannabis smoking shows a dose-response relation with pulmonary risk in the same way that tobacco smoking does. Although problems of cannabis use can arise at any level of use, however low, cannabis use disorders and other problems are more likely to arise in long term, heavy daily users than in casual, infrequent users. (Winstock, et al., 2010). Longitudinal association between cannabis use and mental health has been studied by the researchers. Cannabis use is a known risk factor for a range of mental health problems (van Gastel et al., 2014). Cannabis use has been associated with several adverse life outcomes including unemployment, legal problems, dependence and early school leaving (Serafini et al., 2013). Furthermore, Monshouwer and colleagues (2006) specify that cannabis use is associated with aggression and delinquency. In addition Fergusson and Boden (2008) point out that greater welfare dependence and lower relationship and life satisfaction associated with cannabis abuse. Majority of studies have suggested a significant cognitive decline in cannabis abusers compared to non-abusers and healthy controls (Shrivastava et al., 2011; Solowij, 1988). According to Kalant (2004) Cannabis use has been linked to a number of both short- and long-term health consequences, including depression, paranoia, learning problems, memory and attention deficits. In addition Cannabis use also causes symptoms of depersonalization, fear of dying and irrational panic ideas (Khan & Akella 2009). Also cannabis use significantly increase the risk for manic symptoms (Henquet, Krabbendam & Graaf, 2006) and mania (Leweke & Koethe, 2008). Evidence indicates that cannabis use is considerably associated with both attempted and completed suicides among healthy youths (Serafini et al., 2013; Price et al., 2009). Cannabis intoxication can occur shortly after cannabis use. The intoxication by cannabis is associated with subjective symptoms of euphoria, perceptual distortion, continuous giggling, sedation, lethargy, impaired perception of time, difficulties in the performance of complex mental processes, impaired judgment and social withdrawal (Crippa et al. 2012). Some clinicians have noticed panic attacks with cannabis intoxication. Cannabis intoxication symptoms are usually gone after a maximum of one week abstinence (Lishman, 1988). Heavy cannabis use could lead to an ‘amotivational syndrome which has been described as personality deterioration with loss of energy and drive to work (Tennant & Groesbeck, 1972; Johns, 2001). Cannabis-induced amotivational syndrome negatively impacts on volition, self care and social performance. Cannabis-induced psychotic disorder (CIPD) refers to psychotic symptoms that arise in the context of cannabis intoxication (Morales-Muñoz et al., 2014). Cannabis use is a risk factor for the development of incident psychotic symptoms (Arendt et al, 2005; Kuepper et al., 2011) and exacerbates psychosis (Hall et al., 2004). Hall and team (2004) state that cannabis use can precipitate schizophrenia in vulnerable individuals. Deficits in prepulse inhibition (PPI) and cannabis abuse are consistently found in schizophrenia (Morales-Muñoz et al., 2015). Cannabis use in adolescence leads to a two to three fold increase in relative risk for schizophrenia or schizophreniform disorder in adulthood (Arseneault et al., 2004). The abuse of cannabis by patients with psychiatric disorders such as schizophrenia and mood and anxious disorders has a negative impact both in the acute and advanced stages of these conditions (Diehl, Cordeiro &, Laranjeira, 2010). Exposure to marijuana during a critical period of neural development may interrupt maturational processes (Jacobus et al., 2009). Adolescents appear more adversely affected by heavy use than adults (Schweinsburg, Brown & Tapert , 2008). Chronic cannabis use may alter brain structure and function in adult and adolescent population (Batalla et al., 2013). Sami and colleagues (2015) suspect cannabis use may be associated with dopamine signaling alterations. Fontes and team (2011) point out that cannabis use has been associated with prefrontal cortex (PFC) dysfunction. Arseneault and colleagues (2004) were of the view that cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths. Consequently Moore and team (2007) emphasize that sufficient evidence to warn young people that using cannabis could increase their risk of developing a psychotic illness later in life. According to El Marroun and team (2009) maternal cannabis use, even for a short period, may be associated with several adverse fetal growth trajectories. Cannabinoids have the ability to cross the placental barrier to the foetus and are detectable in the breast milk of mothers who use cannabis (Liebke, 2001). Current evidence indicates that cannabis use both during pregnancy and lactation, may adversely affect neurodevelopment, especially during periods of critical brain growth both in the developing fetal brain and during adolescent maturation, with impacts on neuropsychiatric, behavioural and executive functioning. (Jaques et al., 2014). Prenatal marijuana exposure is associated with adverse perinatal effects (Astley & Little, 1990).
