The evidence for this is mixed, however . Whereas medical users report that alleviation of acute symptoms of these disorders was a primary motivation for permit applications , a systematic review by Walsh et al. reported that this was not consistently observed across credible studies. Of course, marijuana use itself may constitute a risk factor for suicide apart from alleviating symptoms related to depression and anxiety, at least among some populations and for some levels of suicidality . A meta-analysis by Darvishi, Farhadi, Haghtalab, and Poorolajal supports the strong consensus that alcohol use disorder “significantly increases the risk of suicidal ideation, suicide attempt, and completed suicide.” With respect to medical marijuana, of course, the theoretical prediction depends on whether marijuana is used in addition to or instead of alcohol. If marijuana and alcohol use are combined, one might expect no change in suicide risk or even an increase in suicide following legalization. If marijuana replaces alcohol, on the other hand, one might expect a decrease in suicide risk following legalization. Self-reports by medical users in California and Canada indicate that a substantial proportion substitute marijuana for alcohol and other drugs. Since the instruments included items about patients’ potentially criminal behaviors, self-reports are potentially biased. With a few exceptions, opportunity pathways have received less attention in the suicide literature. Noting that suicide risk is highest when the victim is alone in the absence of guardians who would otherwise intervene , Chew and McCleary use the routine activity theory to explain why risk is relatively lower on weekend days, when other household members are more likely to be present, and relatively higher on Mondays, when other household members are likely to be out of the home at school or work. By analogy,vertical grow system if access to medical marijuana obviates the need to leave home, one might expect a lower suicide risk following legalization.
If medical users substitute marijuana for alcohol, moreover, legalization may result in less time spent in licensed alcohol establishments. Anderson, Hansen, and Rees use this argument to explain their finding of a reduction in motor vehicle fatalities following legalization. Firearms access is a relevant opportunity pathway. The positive correlation between firearms access and suicide risk has been demonstrated for U.S. metropolitan areas and counties . These correlations are subject to the ecological fallacy, however. At a disaggregated level, compared with matched controls who live in non-gun households, individuals who live The 1993 Brady Handgun Violence Prevention Act prohibits the purchase of guns by individuals who are addicted to controlled substances. Though used for legal medical purposes, marijuana remains a controlled substance under U.S. law.1 Since California medical marijuana users were not allowed to purchase firearms in 1997, and since California firearms regulations are relatively strict, we expect a reduction in suicide risk following legalization. In sum, in 1996, California legalized marijuana use for medical purposes. Implementation was abrupt and uniform, presenting a natural experiment that we take advantage of in order to estimate the causal effect of a medical marijuana initiative on suicide risk. In the current study, we aggregate total, gun, and non-gun suicides by state for the years 1970–2004. Using a Synthetic Control Group quasi experimental design , we construct a control unit for California from time series of the 41 states that did not legalize marijuana during the time frame. We interpret post-intervention differences for California and its synthetic control time series as the effects of the medical marijuana law on suicide. Significance of the effects is assessed with permutation tests. In 1996, California voters passed an initiative Proposition 215, which legalized marijuana use for medical purposes. Because the Proposition was implemented in an abrupt and uniform manner, legalization presented a “natural experiment.”
To estimate the causal impact of legalization on suicide, annual time series of total, gun, and non-gun suicides were analyzed by comparing California with an estimated counterfactual state in a Synthetic Control Group design. The synthetic control time series for California were constructed as a weighted combination of 41 states that did not legalize medical marijuana during the time frame. Post-intervention differences between California and its constructed control time series were interpreted as the causal effect of the medical marijuana law on suicide. The statistical significance of these effects was assessed with permutation tests. Findings reveal that rates of total suicide and gun suicide dropped significantly in the aftermath of Proposition 215. Findings also reveal, however, that legalization’s impact on non-gun suicides is considerably smaller, and arguably no different than what would be expected to occur by chance. Confidence in these findings is underscored by the methodological approach undertaken in the study. A strength of the Synthetic Control Group Design is that it allows us to examine the net effect of medical marijuana legalization on suicide. Despite the strengths of this design, important limitations remain, many of which present opportunities for future directions in research. Because we examine suicide trends over eight post-intervention years, we are fairly confident that the effects are permanent. Because our time series end in 2005, on the other hand, it is difficult to generalize our theoretical result to subsequent years. We are limited by the fact that medical marijuana laws began to proliferate across the U.S. after 2005, threatening to contaminate the “donor pool” of untreated states. In virtually all the states that legalized medical marijuana after 2005, moreover, reforms were not implemented abruptly or uniformly, making confident causal interpretations more difficult. Another limitation that presents a future direction relates to the mechanisms that may account for the findings of the study. What are the mechanisms responsible for the sharp decline in total, but especially gun, suicides following medical marijuana legalization in California?
We proposed mechanisms related to the substitution of marijuana for alcohol and other related substances; marijuana use itself, which may reduce actual motivation for suicide; the inability of medical marijuana patients to purchase firearms; and changes in the culture of recreational substance use, leading to fewer unsupervised opportunities to commit suicide in the home. Each of these pathways should be tested, although many will require additional data collection. For example, one likely fruitful research direction would be to collect annual data on alcohol consumption in California and assess whether it is a plausible mechanism by which medical marijuana legalization could cause a reduction in gun suicides. Beyond adjudicating these various pathways, testing mechanisms could yield insight into why we do not find the expected reduction in non-gun suicides following legalization. Unfortunately, we do not have the data to test these mechanisms, yet it will be essential for future researchers to do so. In the U.S., use of prescription pain relievers , also known as prescription opioids and opioid pain relievers, has been increasing dramatically. Worldwide, prescriptions of PPRs have almost tripled since 1990, and the U.S. is a factor in this rise, as it has the highest percapita consumption of PPRs in the past ten years . This increase has become dangerous, as opioid use carries risks that include addiction, sedation, respiratory depression, overdose and death . Between 1999 and 2010, deaths attributed to PPRs rose five times among women and 3.5 times among men . Of all prescription drug OD deaths in the U.S. in 2013, 71.3% involved PPRs . PPRs and marijuana are biologically linked; like PPRs, marijuana induces analgesia, acts on some of the same brain regions, and partly exerts its effects via opioid receptors . This connection is especially relevant due to the changing legal status of marijuana. As of August 2016, 24 states and Washington D.C. had legalized medical marijuana. Between 2007 and 2012, the number of past month marijuana users rose from 5.8 to 7.3% 2013, and between 2001 and 2013, past year adult marijuana use increased from 4.1 to 9.5% in the U.S. . Further, legalization of medical marijuana has been associated with increased odds of marijuana use among adults ,cannabis grow equipment though no consistent association has been determined among youth/young adults . Distinct theories attempt to explain how medical marijuana legalization affects use of substances other than marijuana. The relationship between different substances can be impacted by 1) change in cost of a substance, 2) policy alterations that influence availability of a substance, 3) shifts in legal consequences of using a substance, and/or 4) the psychoactive/pharmacological effects of a substance . More U.S. states are legalizing medical marijuana , and marijuana shares some psychoactive/pharmacological effects with PPRs. The substitution theory postulates that there is a substitution effect, whereby an increase in marijuana use coincides with a decrease in the use of other substances – in this case, PPRs . There are logical reasons why individuals would opt to use marijuana instead of PPRs.
With the new legal status of medical marijuana, individuals can access it through medical dispensaries and enjoy a lower legal risk if they live in a state where it is legalized. Individuals also report switching to marijuana for pain control because when compared to prescription drugs, marijuana has fewer side effects and withdrawal symptoms . Studies supporting the substitution effect have demonstrated that either increases in the use of marijuana or the legalization of medical marijuana is associated with reductions in opioid use, hospitalizations for opioid dependence/abuse, PPR ODs, and opioid OD mortality . In contrast to the substitution effect, there may be a complementary effect, where an increase in marijuana use is associated with an increase in the use of PPRs . In support of this theory, researchers using National Survey on Drug Use and Health data found a positive association between marijuana and increased use of PPRs . In another study, researchers focused on individuals who were prescribed long-term opioid therapy and found that those who also used medical marijuana presented with greater risk of misusing prescription opioids. Additionally, a prospective cohort study using the National Epidemiologic Survey of Alcohol and Related Conditions data determined that use of marijuana was associated with a greater risk of using non-medical prescription opioids three years later . However, in these studies, researchers did not analyze how co-use of other substances would impact the direction and/or strength of the relationship between marijuana and opioids/PPRs. To determine if there is either a substitution or a complementary effect between marijuana use and PPR use, co-use with other substances needs to be studied. Additionally, there is a strong positive association between nicotine use and PPR use. When compared to non-smokers, tobacco smokers experience more intense and longer lasting chronic pain, as well as a higher frequency of PPR use . Studies have demonstrated an interaction between nicotine and opioids that is associated with an increase in the total consumption of the two substances and contributes to other effects of the drugs . The relationship between the use of these two substances has a basis in the biological connection between them, as the endogenous opioid system is an underlying mechanism for several behavioral outcomes related to nicotine . Like marijuana, nicotine is involved in anti-nociception via endogenous opioid system mediation, suggesting that nicotine is used for the self medication of pain ; and in fact, nicotine heightens the anti-nociceptive effects of both opioids and marijuana . Several studies have documented common use patterns among tobacco, marijuana, and opioids/PPRs . For example, a prospective study of NESARC data demonstrated that early-onset of smoking cigarettes increased the odds of beginning opioid use and that frequency of both cigarette and marijuana use increased the odds of beginning opioid use, re-initiating opioid use after previously stopping, and continuing opioid use among current users . Thus, the three substances share anti-nociceptive actions mediated by the endogenous opioid system, and evidence indicates that marijuana and nicotine use predict opioid use among adults. From 2003 to 2012, NSDUH data revealed a significant increase in the co-use of marijuana and tobacco . Further, smoking tobacco is significantly associated with cannabis dependence . Given the national trend toward marijuana legalization, co-use is likely to increase. Cigarette smokers and marijuana users are a crucial population to study, as nicotine and marijuana share mechanisms of action with each other and with opioids, and use of each substance has been shown to be associated with use of opioids/PPRs . However, whether there is an association between prevalence of marijuana and PPR use among current smokers has not been determined.