The impact of cannabis on cognitive function is a topic of some debate. There are studies that have shown some impairments in heavy users, as well as evidence that it can impair working memory. But, there is not enough information to draw any firm conclusions.
Evidence for impairments in heavy users
Evidence for impairments in cognitive function in heavy cannabis users has been documented. These impairments have been shown to be reversible with abstinence and may be linked to the amount of time spent using the substance. Among other possible implications, these impairments can affect occupational proficiency and interpersonal relationships.
The following table summarizes recent studies evaluating cannabis’s effects on cognition. While the findings are mixed, this information provides a useful overview of the most compelling evidence.
First, the short-term effects of acute cannabis use are evident in information processing and attention. In addition, the effect of cannabis intoxication on memory is dose-dependent. This is evident in both immediate and delayed recall.
Acute effects also impair executive functions, such as decision making and planning. However, evidence for the long-term effects of cannabis is less conclusive. It is unclear whether these effects occur on a subacute or a chronic basis.
Several studies have reported impaired verbal fluency. This has been attributed to the presence of interference. Studies have indicated that cannabis users are more likely to make errors, particularly at short delay intervals.
Despite these findings, the magnitude of impairments varies with study design and the type of impairments measured. For example, a number of studies have found that young adults who have heavy cannabis use have impaired cognitive abilities.
Long-term users performed significantly worse on memory tests. They recalled fewer items on each trial than controls. As the years of use increased, the deficits became more pronounced.
In contrast, studies that required short periods of abstinence revealed a less robust pattern of impairment. Overall, the results showed a general trend of performance impairment in cannabis users.
Research on cannabis’s effects on cognition has been plagued by poor measurement of the duration of cannabis exposure. However, there are some promising recent studies that provide evidence for the effects of heavy use.
The most common deficits are in memory, learning, and processing speed. Short-term effects of acute intoxication have also been observed. Upon abstinence, the basic working and attentional memory capabilities are restored.
In addition, some studies have reported decreased inhibition and concentration. Cannabis intoxication also increases the risk of false memories.
Inconsistent evidence that THC/cannabis impairs working memory
There is inconsistency in the evidence that THC/cannabis impairs working memory. Although the deficits are less severe than those attributed to cocaine, alcohol, and methamphetamine, cannabis use still affects learning and memory. These problems could severely interfere with the daily functioning of heavy users.
Cannabis intoxication also elicits cognitive impairments in a dose-response fashion. This is most obvious when memory performance is evaluated at the immediate versus delayed recall level. Several studies have reported impaired cognitive performance in both chronic and occasional cannabis users. However, the relationship between these impairments and chronic cannabis use is controversial.
Similarly, the evidence regarding the impact of THC/cannabis on decision-making is mixed. Some studies have reported that cannabis use can significantly impair the ability to make judgments and decisions. Others have reported no difference in such performance. The results may be due to missing data or the low sample size.
Using a naturalistic design, a few studies have suggested that CBD can ameliorate the effect of D9-THC on memory and cognition. Other studies have reported a slight to moderate decrease in performance in working memory and episodic memory tasks.
The same research group found that a high-dose of synthetic D9-THC decreased performance on memory and working memory tests. It also indicated that nabiximol, a product with a D9-THC:CBD ratio of 1, attenuates these impairments. A recent longitudinal study also suggests that cannabis exposure and episodic memory task performance are causally related.
Studies assessing the acute effects of cannabis have focused on memory, verbal learning, and speed of processing. Executive functions, such as planning, organizing, controlling emotions, and solving problems, are also affected.
Inconsistencies in the evidence concerning the effects of THC/cannabis on cognitive performance are compounded by the complex nature of the processes involved. As such, more careful and thorough study is necessary to determine the mechanisms that may explain why these deficits exist.
Lastly, although it’s not clear what the most important function of THC/cannabis is, a recent study suggests that altered feedback processing may play a role. This may explain the negative results of attention and working memory tasks.
Evidence for impairments in adolescent-onset users
Adolescent-onset cannabis use is associated with marked declines in verbal IQ, short-term memory and executive functioning. These cognitive impairments are not only limited to memory of real experiences, but are also reversible after abstinence. In addition, adolescent-onset users are more likely to develop a dependence on cannabis.
There are a number of possible neurobiological mechanisms underlying this relationship. Cannabis exposure in experimental animal models has led to important insights into the underlying neurobiology of cannabis exposure. During adolescence, the brain is undergoing a crucial period of neurodevelopment. This may contribute to the cognitive impairments in adolescent-onset cannabis users. However, there are still many questions about the neurobiological causes of cannabis use during adolescence.
Several previous reviews have summarized the evidence from human studies. Some of these studies found hyperactivation in the prefrontal regions during memory processing. Others found a decrease in activation during reward processing. Similarly, adult cannabis users showed a combination of hyper and hypo activation in several brain regions.
The current study tested the association between persistent cannabis use and neuropsychological decline. A bi-directional relationship was found, with a greater decline in IQ in adolescent-onset users compared with adult-onset users. When correcting for pre-use educational scores, adolescent-onset cannabis use was more strongly associated with IQ decline than adult-onset cannabis use.
Cognitive impairments in adolescent-onset marijuana users were assessed in a longitudinal study. Compared with matched control participants, adolescent-onset use was associated with grey matter alterations in the superior temporal gyrus, hippocampus and amygdala. Moreover, adolescent-onset usage is associated with deficits in executive function domains of trial learning.
Studies involving adult-onset users did not find a statistically significant difference in impairment between adolescent and adult groups. Nevertheless, adolescent-onset marijuana use is accompanied by structural changes and a decrease in interhemispheric connectivity.
While adolescent-onset users have been identified as more vulnerable to cognitive impairments, it is not clear whether their impairments are due to a toxic effect of cannabis exposure or to more structural alterations in the developing brain. Considering the increasing prevalence of marijuana use in adolescents, preventing additional cognitive impairments in these users should be a priority.
Preclinical studies of cannabis on the developing brain
The effects of cannabis on the developing brain have been investigated in humans and animals. Some studies have found structural and functional changes.
Structural changes have been observed in the hippocampus, amygdala, cingulate, and insula. These areas are involved in memory processing. Functional connectivity between these regions has been studied in cannabis users.
Adolescent users of cannabis have been shown to have reduced activation in these regions. They also have decreased interhemispheric connectivity. In addition, they have lost gray matter in areas of the medial temporal cortex and the parahippocampus.
Studies have shown that adolescent chronic users have reduced grey matter in the hippocampus and the parietal cortex. This may lead to a disruption in the hippocampal plasticity process.
Animal studies have also documented the negative effects of cannabis on memory and learning. Some studies have reported deficits in male rats. Others have observed impaired memory performance in females. However, these results are inconsistent. Gender-related differences in CB1 receptor density in memory-related areas have been found in both rat and human studies.
Another study compared adolescent abstinence with recent CU and found no significant difference in ROI analysis. CU participants had more extensive periods of abstinence. While the longer abstinence period reduced deficits, the study did not find any significant difference in other areas.
Recent findings have suggested that adolescent cannabis use is associated with decreased activation in memory-related neural substrates. It is likely that cannabis users compensate for these deficits.
There have been numerous reviews of the effects of cannabis on the brain. Many have focused on the adolescent stage. A large number of studies have administered drugs to adolescents, while others have investigated the impact of cannabinoid exposure on the development of the brain.
In adolescent users of cannabis, there is a loss of gray matter in certain areas of the brain. This may be a result of the increased vulnerability of the developing brain during this phase of development.
Longitudinal studies have found that adolescent cannabis use affects white and gray matter structural integrity. This is believed to have implications for endocannabinoid system homeostatism.