To date, little scientific research has been done on how the use of marijuana affects patients with bipolar disorder. Many people with bipolar disorder use marijuana, and there is abundant evidence that it can provoke manic episodes and accelerate phase change. However, it is not yet clear whether the risk of bipolar disorder is increased in people who use marijuana.
Due to the small amount of data available from depression studies, it is not possible to clearly determine the relationship between depression and marijuana use. According to such reports of anxiety states, many marijuana users describe mood improvement. Experimental studies on animals suggest that marijuana components may have antidepressant effects. However, several observations indicate that daily use of marijuana may actually increase or cause symptoms of depression. For example, an Australian study involving 1,601 students found that someone aged 14-15 who had used marijuana at least once a week was twice as likely to develop depression after 7 years as someone who had never blood tuna strain smoked it (even after excluding other physiological and social factors). Young women who used marijuana daily were five times more likely to experience symptoms of depression 7 years later than their non-smoker peers. While such studies do not prove causal links, the dose/effect ratio is of particular interest.
Marijuana is known to exacerbate symptoms and worsen conditions in patients with schizophrenia and other psychotic disorders. The results of several major long-term observations also provide strong indications that marijuana use, especially in early adolescence, may increase the risk of future psychosis.
For example, a study involving 50,000 young Swedish soldiers showed that marijuana smokers were at least twice as likely to develop schizophrenia as those who had never used it. Among psycho bear gummies the most regular users (who admitted to using marijuana more than 50 times), the risk of psychosis increased six times.
Until recently, it was generally accepted that this result reflected an abnormality in the selection principle. People who were already vulnerable to psychosis or in its early stages would be more likely to use marijuana to "tame" voices or get rid of obsessive thoughts. But further analysis of the Swedish study and other observations have shown that the use of marijuana chemicals increases the risk of psychosis, even when several causal factors are taken into account.
Although the cause and effect are still difficult to unequivocally prove, sufficient evidence has been gathered that early use of large quantities of marijuana may not only stimulate psychotic symptoms in already vulnerable individuals, but also cause psychotic symptoms in individuals who otherwise were not predisposed to develop this condition.
Of course, a person's genetic profile can play both a levelling and stimulating role in relation to the impact of marijuana on the patient. For example, people born with a variation in the catechol-O-methyltransferase gene are more likely to develop psychotic disorders. As there is currently no reliable way for clinicians to recognize genetically vulnerable young people early on, the safest approach would be to limit marijuana use to adult patients only.