It’s Complicated: Cannabis and Mental Health

Cannabis leaf

The Cannabis sativa plant contains hundreds of chemicals, including more than 100 cannabinoids. Cannabinoids are a family of compounds, each with different effects. The most familiar cannabinoids are THC (the psychoactive component of marijuana) and CBD (cannabidiol), which is not psychoactive. “Marijuana” generally refers to the components of (and products made from) the Cannabis sativa plant, which are highest in THC. In addition to the various cannabinoids, the cannabis plant contains hundreds of other chemicals, making its potential risks and benefits very difficult to study. Complicating matters further, there are numerous distinct strains of MJ, containing varying mixes of the many compounds. 

A few decades ago, researchers discovered the endocannabinoid system (EDS), comprised of our body’s own natural cannabinoids and cannabinoid receptors in the brain and throughout other parts of the body. This is part of a complex regulatory system that can be thrown off by the introduction of exogenous (outside) cannabinoids.

Synthetic cannabinoids are dangerous. These consist of a wide and ever-changing variety of unregulated lab-manufactured chemicals that are then sprayed on dried random plant material to be smoked, or sold in liquid form for vaping. Examples include K2, Spice and Scooby Snax.  

Regarding medical marijuana laws, there are no current FDA-approved therapeutic indications for marijuana or THC for psychological conditions. One CBD product, Epidiolex, is FDA approved only for specific types of epilepsy. Several regulated synthetic cannabinoids are approved for nausea/vomiting due to chemotherapy and loss of appetite/weight loss related to HIV/AIDS.

There is much we don’t know about the psychological effects of cannabis. I will attempt to briefly summarize the current state of knowledge.  

With more states legalizing the use of marijuana, along with its potential attraction as a “natural” or “herbal” remedy, the perception of its risks is changing. Many do not understand the very real chance of developing cannabis use disorder (CUD). Good evidence shows that approximately 9% of regular cannabis users will develop addiction. The rate is significantly higher in those who begin using before the age of 18; in this population, the addiction rate is as high as 17%. Other predisposing factors include regular use, heavy use, a history of childhood anxiety, ADHD, and a family history of substance abuse. Cannabis withdrawal symptoms, which can be long lasting, make it especially difficult to stop using and to maintain abstinence. These include insomnia, anxiety, depressed mood, irritability, and craving to use. Given nationwide increases in use, decreases in perceived risk, legalization and increased access, and continuing increases in THC concentrations, it is important that people understand that marijuana is, in fact, addictive. THC concentration has gone from around 2% before the 1990s to as high as 28% now (and higher with “dabbing,” some edibles etc.).

Children, adolescents and young adults seem to be most at risk of longer-term adverse effects of using marijuana, primarily because the brain continues active development until at least age 26. Cannabinoid receptors are present throughout multiple brain regions, and chronic cannabis use causes neurobiological changes in these pathways. This puts youth at higher risk of developing addiction as well as potentially permanent changes in IQ and cognitive capacity in general. In addition, marijuana’s effects on the developing brain seems to put younger users at risk for developing a chronic psychosis syndrome.

The association between cannabis use and psychosis is well documented. Cannabis-induced psychosis (CIP) presents with symptoms such as agitation, anxiety, paranoia, and mood swings. In most cases, CIP resolves completely. However, a substantial number of those with CIP, possibly up to 45%, go on to develop persistent psychotic disorders. Studies suggest that adolescents may be at an especially high risk to developing a schizophrenia-like disorder after an episode of CIP, up to 2-6 times the risk of adults. One clear risk factor for developing a persistent psychotic disorder is genetic vulnerability, including a family history of psychotic disorders. People who experience paranoia and anxiety with marijuana use may be at higher risk as well. Other risk factors include early onset of cannabis use, early age of first psychotic episode, longer period of cannabis use, and higher THC dose. Perhaps the most important factor is continued use after the first psychotic episode. The risk of developing a chronic psychotic disorder is substantially reduced if abstinence is achieved and sustained after the first episode of CIP. 

Some studies have linked regular marijuana use to impairments in cognitive functions such as memory, attention, motivation, and learning. Strong evidence also points to lower educational achievement and income levels with regular use.    

In terms of mood, some people use cannabis in the hopes that it will relieve depression. Our endogenous endocannabinoids can cause positive mood states, and users of cannabis often report a sense of well-being or euphoria. However, at this time, studies have not shown evidence for anti-depressant effects of marijuana and have instead suggested the opposite. Again, young people are more at risk. Although the evidence is not as strong as it is for psychosis, cannabis use in adolescents seems to be associated with depression and suicidal ideation, especially with earlier onset of use, more frequent use, and longer-term use, as well as in those with genetic vulnerability to psychiatric disorders.  

In people with pre-existing anxiety and/or mood disorders, prolonged marijuana use (6 months +) has been associated with an increased number of depressive symptoms, increased symptom severity and worsened outcome in several studies. It is thought that marijuana use may interfere with the efficacy of treatment for these disorders. Cannabis may have acute mood elevating effects in some people, mediated through the brain’s endocannabinoid system, but this doesn’t seem to be a sustainable benefit.

Anxiety is one of the most common reasons people give for their marijuana use, describing a sense of calm and relaxation. The endocannabinoid system (EDS) appears to be involved in the regulation of fear and anxiety, so there is some basis for this idea. However, there is no clear scientific evidence of the efficacy of plant-based marijuana in treating anxiety disorders, and, in fact, it can have an adverse impact. 

As mentioned above, the Cannabis sativa plant contains many compounds, with different ratios between strains. For THC, lower doses may reduce anxiety, while higher doses can worsen anxiety and even cause paranoia (especially in susceptible people). Cannabidiol (CBD), on the other hand, appears to have an overall anxiety-lowering effect. Strains with a higher THC: CBD ratio tend to be more likely to cause anxiety, and vice versa.    

There is also the issue of long term vs. short term efficacy. For some people, marijuana may act to reduce anxiety in the short term, but tolerance can develop over time, reducing efficacy in the longer term. Tolerance can develop, chronic use seems to alter brain stress response systems by disrupting our natural EDS system, and anxiety increases with discontinuation. Therefore, marijuana is not a sustainable long-term solution to address anxiety.

A few small studies suggest possible benefits of specific cannabinoid compounds for some anxiety disorders, including PTSD-related sleep disturbance (including the synthetic cannabinoid, Nabilone), generalized anxiety disorder (Nabilone), and social anxiety disorder (CBD), but the evidence is limited and does not address the effects of longer-term use. And the science is even less clear for plant-based cannabis. 

Also, there are significant individual variations in how marijuana affects people, which are not fully understood. In susceptible people, MJ use can precipitate acute intense anxiety, panic, distrust, and paranoid thoughts; as noted above, these individuals also seem to be a higher risk for psychosis, probably related to genetic factors.

Many people use marijuana at bedtime to help with sleep. An internet search of marijuana and sleep brings up multiple websites describing the benefits of marijuana use in addressing insomnia. However, there is not much in the way of recent evidenced-based guidance about marijuana’s effects on sleep. Studies from the 1970s, looking at effects of the cannabis plant, suffered from methodological issues and showed mixed results. Some studies suggest that, in low doses, cannabis may be sedative, while moderate-to-high doses may be stimulating. Some studies show an increase in deep sleep initially, but this was not a sustained effect with ongoing use. In contrast, tolerance seems to develop, prompting people to use larger and larger doses to get the sleep-promoting effect.

More recently, some research has looked at distinguishing the effects of THC from CBD. CBD, for example, seems to affect sleep differently, with lower doses worsening sleep, while higher doses (160mg) promoting sleep.  

In addition, there is good evidence that sleep disturbance after discontinuation of cannabis is common, tends to be severe, and can be sustained, lasting up to 45 days after discontinuing use. Cannabis withdrawal has been associated with initial insomnia, decreased time asleep, and strange dreams (REM rebound). This makes it very difficult to sustain abstinence, increasing the risk for developing addiction.

We will certainly be learning more in the years to come.  In the meantime, here are a couple of good science-based websites to explore: 


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