Adolescent Cannabis Use

In 2022, cannabis use had an estimated lifetime prevalence of 38% among 12th grade students in the United States, a 17% increase compared to 1992. Additionally, while the prevalence of use remained relatively steady among youth aged 12–17 years over the past decade, rates have continued to rise among older youth and emerging adults aged 18–25 years. These older youth also have the highest prevalence of cannabis use compared to other age groups. Although not all individuals who consume cannabis develop a CUD, broadly conceptualized as a pattern of continued cannabis use despite the development of clinically significant problems, a significant number do. Epidemiologic data of the prevalence of CUD in youth are limited and largely predate broad adoption of medical and recreational marijuana laws in the United States. However, a recent meta-analysis which included youth and adult studies reported that among individuals who used cannabis, 22% met criteria for CUD (95% CI 18%–26%). CUD was most prevalent in young adults, with the highest risk of CUD (41.1%, 95% CI 38.4%–43.8%) among the cohort of 21-year-old emerging adults.

The complex biological properties of cannabis and cannabinoid products and their potential medicinal or adverse effects and their relation to the developing brain are still actively being explored. Of the more than 500 chemicals in the cannabis plant, Δ9-tetrahydrocannabinol (THC) is known to be the most abundant intoxicating cannabinoid. Although most individuals who consume cannabis use full-spectrum cannabis products, THC has been shown to be associated with adverse mental health outcomes. Moreover, the higher the THC potency, the greater the risk of developing CUD and poorer mental health outcomes. The potential of THC to impact neurodevelopment is thought to be mediated through its direct effects on the endocannabinoid system. This modulatory system plays a vital role in regulating neural differentiation and migration, axon guidance, synaptogenesis, and myelination, as well as neurotransmitter system development. Consequently, cannabis exposure during neurodevelopment, whether through exposure in early life (prenatal or childhood) or adolescent use, has the potential to alter the endocannabinoid system. Such exposure could thus impact the development of neural pathways that mediate reward; emotional regulation; and multiple cognitive domains including executive functioning and decision making, learning, abstraction, and attention, all processes central to substance use disorder and other psychiatric disorders.

Growing concerns regarding adolescent-onset cannabis use relates to its association with the increased prevalence and severity of mental health disorders, including psychosis, depression, anxiety, bipolar disorder, and other substance use disorders. Youth who use cannabis are also more likely to endorse suicidal behavior including suicide attempts. Of the various mental health challenges, significant attention has focused on the co-occurrence of cannabis use and psychosis. Though significant debates remain regarding their causal relationship, the literature has highlighted factors of cannabis use, including frequency, potency, and earlier age of onset, as risk factors for psychosis. Moreover, a recent study of over 6 million individuals in Denmark showed that CUD was a major risk factor for schizophrenia, particularly among young males. While Hjorthoj et al., were not able to establish causality or conclude CUD was a modifiable risk factor, the authors estimated that as many as 30% of cases of schizophrenia among men aged 21–30 years might be prevented by averting CUD. The relationship between cannabis use and mental health is likely bidirectional, with shared common predisposing risk factors, neurobiological perturbations and overlapping genetics that may contribute to high rates of comorbidity.

Cannabis Use Disorder Risk

In addition to psychiatric comorbidities, several risk factors for the development of CUD have been identified, including social factors, environmental conditions, and personality traits (Figure 1). However, large-scale studies consistently report two main factors associated with CUD risk. The first is age, both for the onset and frequency of use at younger age. Similar to a number of other psychiatric conditions, CUD risk peaks in adolescence, with most CUD cases becoming evident between ages 18–30 years. Those who start using cannabis prior to age 16 years are at the highest risk of developing CUD. Moreover, youth who initiate use before the age of 18 years are significantly more likely to develop CUD, with substance-related problems continuing into adulthood, and to experience adverse psychiatric and personal outcomes. The risk of developing CUD also increases significantly among youth who use cannabis at least weekly, with the highest prevalence among youth who use cannabis daily. One large-scale study reported increased use frequency associated with an 8–17-fold increased risk for developing CUD.

FIGURE 1. Early predictors of cannabis use and presentations and outcomes of cannabis use disorder

As noted above, the increased vulnerability to CUD following early use has implicated developmental perturbations in mesocorticolimbic brain regions, which mediate reward and emotion processing as well as cognitive control. Prospective longitudinal neuroimaging studies from the European IMAGEN consortium of teens from age 14 revealed that adolescent cannabis use is associated with accelerated cortical thinning, which was correlated with impulsive behavior. This finding of cortical thinning is consistent with a number of cross-sectional neuroimaging studies. Furthermore, amygdala reactivity during adolescence prospectively predicts cannabis use and CUD. Neuroimaging studies in adult individuals diagnosed with CUD also report similar mesocorticolimbic alterations. More recent ongoing longitudinal neuroimaging efforts includes the long-term Adolescent Brain Cognitive Development (ABCD) study that has tracked youth from age 9–10 years. Emerging data has so far revealed that early initiation of cannabis use and CUD is predicted by early childhood adversity, early initiation of tobacco and alcohol use, and maternal prenatal cannabis use. However, the causal relationship between these factors and cannabis use remains challenging to establish.

The second factor consistently associated with the risk of CUD is biological sex. CUD rates are normally higher among male individuals, but marked gender differences in use patterns, motivations, and CUD presentation are noted. For example, male individuals are more likely to be diagnosed with CUD and show higher frequency of use. However, when controlling for frequency of use, CUD incidence does not differ between genders. Female individuals show faster CUD progression, referred to as telescoping. Similarly, female individuals with CUD may be more likely to show increased withdrawal symptoms, comorbidity with anxiety or mood disorders, and interpersonal difficulties. These data suggest that cannabis and certain products may have different subjective and physiological effects in male and female individuals, which ultimately may influence the development of CUD. Importantly, the sex gap for CUD is narrowing, which might be due to higher consumption by young females or the higher potency of products used today.

A Changing Product and Use Pattern in the Cannabis Landscape

Commercialization of cannabis products in legal markets has led to a sharp rise in THC potency, as well as availability and utilization of high-THC products, such as dab pens, wax, or shatter, among youth. Though recent studies have shown that high THC potency may be associated with increased risk of developing CUD, the neurodevelopmental impact of using current THC concentrates during adolescence remains understudied. To date, the integration of research findings has also been compromised by diverse and inconsistent measures of exposure. This is in part due to the wide array of cannabis products, with many individuals regularly using more than one type of product. Moreover, very limited information is known about the type of cannabis and cannabinoid products being used including a recently identified rare but extremely potent cannabinoid, tetrahydrocannabiphorol (THC-P), now widely available commercially. Information is also lacking regarding the proliferation of hemp-derived products that circumvented state and federal laws in manufacturing cannabinoids such as Δ⁸-THC other THC analogs (e.g., Δ¹⁰-THC and hexahydrocannabinol [HHC]), through the chemical conversion of cannabidiol, a non-intoxicating cannabinoid. The same challenges are evident with precursor products such as THC-acid (THCA) which converts to Δ⁹-THC upon heating. Though adolescents and young adults often think that these popular new THC-analogs are “healthier,” they can produce cannabimimetic effects similar or greater than Δ⁹-THC. The mental health implications expected with these new THC analogs requires significant monitoring and research attention.

Another factor critical for CUD is the developmental pattern of cannabis use relevant to severity of use. Most epidemiologic studies query the prevalence of cannabis use within a set time frame, most often past 30-day, past year, or lifetime. As noted above, the frequency of cannabis use is associated with increased risk of developing a CUD, but some clinicians misapply frequency of use as a measure of CUD severity. Consideration of factors used with identifying alcohol use disorder may yield new insights into high-risk patterns of cannabis use and the development of CUD. For instance, cannabis use in the morning (e.g., “eye opener,” “wake and bake”) may be more indicative of problematic use. Such information is, however, not often considered within screening and diagnostic constructs of CUD. Similarly, binge patterns of cannabis use have not been characterized, and the impact of episodic consumption of large amounts of high potency THC on the development of CUD is unknown. Alternatively, improved characterization of an individual’s use beyond timeline follow-back may be accomplished via boarder adoption of subjective measures of cannabis use, though further studies are needed to validate such measures and establish a consensus guideline for future research.

Insights from Preclinical Models

Multidisciplinary efforts are required to address the critical need to understand the neurodevelopmental impact of the proliferating diverse cannabis and cannabinoid products. Animal models therefore remain a critical resource to interrogate the causal impact of cannabinoids on the developing brain that may be relevant to the genesis of CUD. Preclinical studies to date have provided unique insights demonstrating that prenatal and adolescent THC exposure increases anxiety behavior, deficits in sociality, increased depressive-like behavior, addiction vulnerability, and cognitive deficits. Deficits are tied to perturbations in mesocorticolimbic (prefrontal cortex, nucleus accumbens, and amygdala), gene expression, protein, and cell morphology. For example, rodent models of adolescent THC exposure demonstrate reduced morphological complexity of pyramidal cortical neurons, which would be in line with cortical thinning seen in human adolescent studies. These animal models have also elucidated unique neurobiological underpinnings associated with high potency THC during adolescence on brain and cognitive behavior relevant to CUD risk.

There are still, however, substantial translational gaps between existing animal models and the current cannabis landscape. For example, the majority of preclinical studies utilize parenteral administration of cannabinoids to determine the impact on behavioral, physiological, and molecular phenotypes. This is due to the challenge that rodents do not readily self-administer THC through traditional intravenous preclinical “addiction” methods and often find THC aversive. Although injections of THC have revealed important relationships between drug and outcomes, human users mainly smoke, vape, or consume edible cannabis products. Novel rodent data indicate that vaporized THC produces different peak plasma and brain concentrations, metabolism profiles, molecular, and behavioral outcomes compared to injected THC. Furthermore, vaporized cannabis extracts are self-administered by rats and adolescent animals will volitionally consume edible THC gelatin. These novel translational models create new inroads to better understand how developmental cannabis exposure and self-administration impact the trajectory of brain processes and behavior relevant to CUD risk.

To maximize the potential of novel translational models, both the clinical and preclinical fields need to standardize metrics of key outcomes. This includes determining fundamental pharmacological metrics (e.g., peak plasma concentrations, metabolite profile) to better compare the potency impact in animal models versus humans, as well as setting standard translationally relevant behavioral outcomes that recapitulate phenotypes observed in humans. Integration of longitudinal designs should test behaviors across development into adulthood using doses and routes of administration relevant to the current landscape seen in human cannabis consumption. These preclinical efforts will accelerate our mechanistic understanding as to how developmental THC and cannabinoids causally influence phenotypes relevant to psychiatric and CUD risk.

Addressing Adolescent Cannabis Use

Another important factor in tackling the changing cannabis landscape is treatment. There is currently an unfortunate disparity between the estimated prevalence of CUD and the number of youths who receive evidence-based treatment. Treatment strategies are currently limited and consist mainly of motivational enhancement and cognitive behavioral therapies. Given that the increased potency of cannabis and cannabinoid products is expected to increase CUD risk, it is disturbing that less than 10% of youths who meet the criteria for a substance use disorder, including CUD, receive treatment. More recently, there has been a decline in treatment admissions for CUD among youths across the United States, including in states with recreational marijuana laws.

Even when treatment is available, adolescents often do not engage due to lack of perceived need for treatment. With the expansion of recreational laws and statutory classification as “medicinal” at the state level, perceived harmfulness of cannabis use continues to decline. In fact, some studies suggest that youths perceive concentrated THC products, particularly vapes or dab pens, as less harmful than combustible plant-based products. This is further complicated by the perception that cannabis use is helpful for mental health problems that may be exacerbated by cannabis use. Broad education efforts are needed, but educating youths about cannabis is complicated by the extensive amount of information and misinformation available online and via social media. Individualized interventions may be better targeted by primary care and mental health professionals, who can address individual and family factors that often contribute to comorbid mental health problems as well.

Challenges in treatment provision also exist. Of the few evidence-based interventions currently used to treat CUD, their availability and efficacy remain limited. This is paired with potential lack of insight into cannabis-related problems. For example, self-reported physiologic changes consistent with tolerance and withdrawal are often not recognized as problems related to cannabis use. Insufficient clinical screening and unrecognized substance-related problems may also result in clinicians missing problematic cannabis use entirely or inaccurately classifying adolescent cannabis use as misuse rather than a CUD. Further, clinicians may not screen for substance use problems because of a lack of available resources or programs to which youth may be referred.

A multifaceted approach is required to address this gap in care, including broader implementation of universal and selective interventions. Risk and protective factors for the onset of youth cannabis use can be conceptualized using the socio-ecological model, which posits that factors at multiple levels, including individual and peer, family, school, and community, contribute to cannabis use. Using this framework, current evidence supports the broad implementation of universal and selective interventions that enhance protective and reduce risk factors. This may include implementation of evidence-based interventions at the institutional (e.g., school) or community level. Integration of behavioral interventions into primary care, social work, and school-based settings presents a significant opportunity to leverage current infrastructure and provide treatment where youth are already engaged in other services. Moreover, as states vie to leverage tax dollars from the growing cannabis industry, a significant portion of such funds must be used for early intervention/prevention strategies to reduce the impact of cannabis on the developing brain.

Conclusions

The relationship between developmental cannabis, the impact of high potency products, and increased risk of developing CUD and mental health problems must be taken seriously, especially in light of the current mental health crisis. The plasticity of the developing brain offers windows of opportunity for prevention and early intervention to change that trajectory. Clearly new treatment strategies are needed to address the mounting challenge of CUD risk in teens and young adults. While data accumulated over the past decades about the effects of now “low dose” THC has been very valuable, significant research efforts in preclinical models are needed, focused on THC potency relevant to today’s products. Additionally, longitudinal studies such as ABCD should be able to provide important insights about factors related to resilience that may also help guide the development of intervention strategies. Altogether, the combined longitudinal, clinical and preclinical efforts will help provide unprecedented knowledge to mitigate the trajectory of CUD and related psychiatric disorders, both of which have a strong neurodevelopmental etiology.

Adolescent Cannabis Use

In 2022, approximately 38% of 12th-grade students in the United States reported lifetime cannabis use, representing a 17% increase since 1992. While cannabis use among youth aged 12–17 years has remained relatively stable over the past decade, rates have continued to rise in older youth and young adults aged 18–25 years. This older age group demonstrates the highest prevalence of cannabis use compared to other demographics. Not all individuals who use cannabis develop a Cannabis Use Disorder (CUD), defined as a pattern of continued cannabis use despite significant clinical problems; however, a substantial number do. Epidemiological data on CUD prevalence in youth are limited, largely predating the widespread legalization of medical and recreational cannabis in the United States. A recent meta-analysis, which included both youth and adult studies, indicated that 22% of individuals who used cannabis met the criteria for CUD, with a higher risk observed in young adults. Specifically, 41.1% of 21-year-old emerging adults exhibited the highest risk of CUD.

The complex biological properties of cannabis, cannabinoid products, and their potential medicinal or adverse effects on the developing brain are subjects of ongoing research. Of the over 500 chemicals in the cannabis plant, Δ9-tetrahydrocannabinol (THC) is recognized as the most abundant intoxicating cannabinoid. While most individuals consume full-spectrum cannabis products, THC has been linked to negative mental health outcomes. Furthermore, higher THC potency is associated with an increased risk of developing CUD and poorer mental health. THC's potential impact on neurodevelopment is believed to occur through its direct influence on the endocannabinoid system. This system is crucial for regulating neural differentiation, migration, axon guidance, synaptogenesis, myelination, and the development of neurotransmitter systems. Consequently, cannabis exposure during neurodevelopment, whether in early life (prenatal or childhood) or during adolescence, can potentially alter the endocannabinoid system. Such alterations could affect the development of neural pathways involved in reward, emotional regulation, and various cognitive functions, including executive functioning, decision-making, learning, abstraction, and attention—all processes central to substance use disorders and other psychiatric conditions.

Increasing concerns regarding adolescent-onset cannabis use relate to its association with a higher prevalence and severity of mental health disorders, including psychosis, depression, anxiety, bipolar disorder, and other substance use disorders. Young individuals who use cannabis are also more likely to report suicidal behaviors, including suicide attempts. Among various mental health challenges, significant attention has focused on the co-occurrence of cannabis use and psychosis. Although debates persist regarding their causal relationship, the literature identifies cannabis use factors such as frequency, potency, and earlier age of onset as risk factors for psychosis. A recent study involving over 6 million individuals in Denmark revealed that CUD was a major risk factor for schizophrenia, particularly among young males. While causality was not established and CUD was not confirmed as a modifiable risk factor, the authors estimated that preventing CUD could avert up to 30% of schizophrenia cases among men aged 21–30 years. The relationship between cannabis use and mental health is likely bidirectional, with shared predisposing risk factors, neurobiological disturbances, and overlapping genetics potentially contributing to high rates of comorbidity.

Cannabis Use Disorder Risk

Beyond psychiatric comorbidities, several risk factors for the development of CUD have been identified, including social factors, environmental conditions, and personality traits. However, large-scale studies consistently highlight two primary factors associated with CUD risk. The first is age, specifically the age of onset and the frequency of use at a younger age. Similar to many other psychiatric conditions, CUD risk peaks in adolescence, with most cases becoming evident between 18–30 years. Individuals who begin using cannabis before age 16 are at the highest risk of developing CUD. Moreover, youth who initiate use before 18 are significantly more likely to develop CUD, experience substance-related problems continuing into adulthood, and face adverse psychiatric and personal outcomes. The risk of developing CUD also increases significantly among youth who use cannabis at least weekly, with the highest prevalence among those who use it daily. One large-scale study reported that increased use frequency was associated with an 8–17-fold increased risk for developing CUD.

The heightened vulnerability to CUD following early use suggests developmental perturbations in mesocorticolimbic brain regions, which govern reward and emotion processing, as well as cognitive control. Prospective longitudinal neuroimaging studies from the European IMAGEN consortium, tracking teenagers from age 14, showed that adolescent cannabis use is linked to accelerated cortical thinning, which correlated with impulsive behavior. This finding aligns with several cross-sectional neuroimaging studies. Furthermore, amygdala reactivity during adolescence prospectively predicts cannabis use and CUD. Neuroimaging studies in adults diagnosed with CUD also report similar mesocorticolimbic alterations. More recent longitudinal neuroimaging efforts, such as the Adolescent Brain Cognitive Development (ABCD) study, have tracked youth from ages 9–10 years. Emerging data indicate that early initiation of cannabis use and CUD are predicted by early childhood adversity, early initiation of tobacco and alcohol use, and maternal prenatal cannabis use. Nevertheless, establishing a causal relationship between these factors and cannabis use remains challenging.

The second factor consistently associated with CUD risk is biological sex. CUD rates are typically higher among males, but notable gender differences exist in use patterns, motivations, and CUD presentation. For instance, males are more frequently diagnosed with CUD and exhibit higher use frequency. However, when controlling for frequency of use, CUD incidence does not differ between genders. Females often demonstrate faster CUD progression, termed "telescoping." Similarly, females with CUD may be more prone to increased withdrawal symptoms, comorbidity with anxiety or mood disorders, and interpersonal difficulties. These data suggest that cannabis and certain products may exert different subjective and physiological effects in males and females, potentially influencing CUD development. Importantly, the sex gap for CUD is narrowing, possibly due to higher consumption by young females or the increased potency of currently used products.

A Changing Product and Use Pattern in the Cannabis Landscape

The commercialization of cannabis products in legal markets has led to a sharp increase in THC potency and the availability and use of high-THC products, such as dab pens, wax, or shatter, among youth. Although recent studies indicate that high THC potency may be associated with an elevated risk of developing CUD, the neurodevelopmental impact of using current THC concentrates during adolescence remains understudied. To date, the integration of research findings has also been hindered by diverse and inconsistent measures of exposure. This is partly due to the wide array of cannabis products, with many individuals regularly using more than one type. Furthermore, limited information is available regarding the type of cannabis and cannabinoid products being used, including a recently identified, rare but extremely potent cannabinoid, tetrahydrocannabiphorol (THC-P), now widely available commercially. Information is also lacking concerning the proliferation of hemp-derived products that circumvent state and federal laws in manufacturing cannabinoids such as Δ8-THC and other THC analogs (e.g., Δ10-THC and hexahydrocannabinol [HHC]) through the chemical conversion of cannabidiol, a non-intoxicating cannabinoid. The same challenges apply to precursor products like THC-acid (THCA), which converts to Δ9-THC upon heating. Although adolescents and young adults often believe these popular new THC analogs are "healthier," they can produce cannabimimetic effects similar to or greater than Δ9-THC. The mental health implications of these new THC analogs require significant monitoring and research attention.

Another critical factor for CUD is the developmental pattern of cannabis use relevant to its severity. Most epidemiological studies inquire about cannabis use prevalence within a specified timeframe, typically the past 30 days, past year, or lifetime. As previously noted, the frequency of cannabis use is associated with an increased risk of developing CUD, but some clinicians incorrectly apply frequency as a sole measure of CUD severity. Considering factors used to identify alcohol use disorder may offer new insights into high-risk patterns of cannabis use and CUD development. For instance, cannabis use in the morning (e.g., "eye opener," "wake and bake") may be more indicative of problematic use. Such information, however, is not often included in CUD screening and diagnostic constructs. Similarly, binge patterns of cannabis use have not been characterized, and the impact of episodic consumption of large amounts of high-potency THC on CUD development remains unknown. Alternatively, a more comprehensive characterization of an individual's use beyond timeline follow-back could be achieved through broader adoption of subjective measures of cannabis use, although further studies are needed to validate such measures and establish consensus guidelines for future research.

Insights from Preclinical Models

Multidisciplinary efforts are necessary to address the critical need to understand the neurodevelopmental impact of the proliferating diverse cannabis and cannabinoid products. Animal models therefore remain a crucial resource for investigating the causal impact of cannabinoids on the developing brain, which may be relevant to the genesis of CUD. Preclinical studies to date have provided unique insights, demonstrating that prenatal and adolescent THC exposure increases anxiety behaviors, deficits in sociality, increased depressive-like behavior, addiction vulnerability, and cognitive deficits. These deficits are linked to perturbations in mesocorticolimbic brain regions (prefrontal cortex, nucleus accumbens, and amygdala), as well as changes in gene expression, protein levels, and cell morphology. For example, rodent models of adolescent THC exposure show reduced morphological complexity of pyramidal cortical neurons, consistent with cortical thinning observed in human adolescent studies. These animal models have also illuminated unique neurobiological underpinnings associated with high-potency THC during adolescence on brain and cognitive behavior relevant to CUD risk.

However, substantial translational gaps persist between existing animal models and the current cannabis landscape. For instance, the majority of preclinical studies utilize parenteral administration of cannabinoids to determine their impact on behavioral, physiological, and molecular phenotypes. This is due to the challenge that rodents do not readily self-administer THC through traditional intravenous preclinical "addiction" methods and often find THC aversive. Although THC injections have revealed important drug-outcome relationships, human users primarily smoke, vape, or consume edible cannabis products. Novel rodent data indicate that vaporized THC produces different peak plasma and brain concentrations, metabolism profiles, and molecular and behavioral outcomes compared to injected THC. Furthermore, vaporized cannabis extracts are self-administered by rats, and adolescent animals will voluntarily consume edible THC gelatin. These novel translational models create new avenues to better understand how developmental cannabis exposure and self-administration impact the trajectory of brain processes and behavior relevant to CUD risk.

To maximize the potential of novel translational models, both clinical and preclinical fields need to standardize metrics for key outcomes. This includes determining fundamental pharmacological metrics (e.g., peak plasma concentrations, metabolite profile) to better compare potency impacts in animal models versus humans, as well as establishing standard translationally relevant behavioral outcomes that mirror phenotypes observed in humans. Integration of longitudinal designs should test behaviors across development into adulthood, using doses and routes of administration relevant to current human cannabis consumption patterns. These preclinical efforts will accelerate mechanistic understanding of how developmental THC and cannabinoids causally influence phenotypes relevant to psychiatric and CUD risk.

Addressing Adolescent Cannabis Use

Another important factor in addressing the evolving cannabis landscape is treatment. There is currently an unfortunate discrepancy between the estimated prevalence of CUD and the number of young individuals who receive evidence-based treatment. Current treatment strategies are limited, primarily consisting of motivational enhancement and cognitive behavioral therapies. Given that increased potency of cannabis and cannabinoid products is expected to elevate CUD risk, it is concerning that less than 10% of youth meeting criteria for a substance use disorder, including CUD, receive treatment. More recently, a decline in CUD treatment admissions among youth has been observed across the United States, including in states with recreational marijuana laws.

Even when treatment is available, adolescents often do not engage due to a lack of perceived need for treatment. With the expansion of recreational laws and statutory classification as "medicinal" at the state level, the perceived harmfulness of cannabis use continues to decline. In fact, some studies suggest that youth perceive concentrated THC products, particularly vapes or dab pens, as less harmful than combustible plant-based products. This situation is further complicated by the perception that cannabis use is beneficial for mental health problems, which may actually be exacerbated by cannabis use. Broad educational efforts are needed, but educating youth about cannabis is complex due to the extensive amount of information and misinformation available online and via social media. Individualized interventions may be more effectively delivered by primary care and mental health professionals, who can address individual and family factors often contributing to comorbid mental health problems.

Challenges in treatment provision also exist. Of the few evidence-based interventions currently used to treat CUD, their availability and efficacy remain limited. This is coupled with a potential lack of insight into cannabis-related problems. For example, self-reported physiological changes consistent with tolerance and withdrawal are often not recognized as problems related to cannabis use. Insufficient clinical screening and unrecognized substance-related problems may also lead to clinicians entirely missing problematic cannabis use or inaccurately classifying adolescent cannabis use as misuse rather than a CUD. Furthermore, clinicians may not screen for substance use problems due to a lack of available resources or programs to which youth can be referred.

A multifaceted approach is required to address this gap in care, including broader implementation of universal and selective interventions. Risk and protective factors for the onset of youth cannabis use can be understood through the socio-ecological model, which proposes that factors at multiple levels—individual, peer, family, school, and community—contribute to cannabis use. Within this framework, current evidence supports the broad implementation of universal and selective interventions that enhance protective factors and reduce risk factors. This may include implementing evidence-based interventions at institutional (e.g., school) or community levels. Integrating behavioral interventions into primary care, social work, and school-based settings presents a significant opportunity to leverage existing infrastructure and provide treatment where youth are already engaged in other services. Moreover, as states aim to leverage tax revenues from the growing cannabis industry, a substantial portion of such funds must be allocated for early intervention and prevention strategies to reduce the impact of cannabis on the developing brain.

Conclusions

The relationship between developmental cannabis use, the impact of high-potency products, and the increased risk of developing CUD and mental health problems must be taken seriously, particularly in light of the current mental health crisis. The plasticity of the developing brain offers opportunities for prevention and early intervention to alter this trajectory. Clearly, new treatment strategies are needed to address the growing challenge of CUD risk in teenagers and young adults. While data accumulated over past decades about the effects of what are now considered "low dose" THC products have been valuable, significant research efforts in preclinical models are now needed, focusing on THC potency levels relevant to today’s products. Additionally, longitudinal studies such as ABCD should provide important insights about factors related to resilience that may also help guide the development of intervention strategies. Altogether, combined longitudinal, clinical, and preclinical efforts will provide unprecedented knowledge to mitigate the trajectory of CUD and related psychiatric disorders, both of which have a strong neurodevelopmental etiology.

Adolescent Cannabis Use

The use of cannabis among 12th-grade students in the United States reached an estimated 38% lifetime prevalence in 2022, marking a 17% increase since 1992. While cannabis use rates for youth aged 12–17 years have remained relatively stable over the past decade, rates have continued to rise among older youth and young adults aged 18–25 years. This older group also shows the highest overall prevalence of cannabis use compared to other age groups. Although not every individual who uses cannabis develops a Cannabis Use Disorder (CUD)—defined as continued cannabis use despite significant problems—a notable number do. Data on CUD prevalence in youth is limited, particularly data from before the widespread legalization of medical and recreational marijuana. However, a recent analysis of studies involving both youth and adults found that 22% of cannabis users met the criteria for CUD. The risk of CUD was highest in young adults, with a 41.1% risk among 21-year-old emerging adults.

The complex biological properties of cannabis, cannabinoid products, and their potential effects on the developing brain are still being actively researched. Among the more than 500 chemicals in the cannabis plant, Δ9-tetrahydrocannabinol (THC) is recognized as the most abundant intoxicating cannabinoid. While most individuals use full-spectrum cannabis products, THC has been linked to negative mental health outcomes. Furthermore, higher THC potency increases the risk of developing CUD and leads to poorer mental health outcomes. THC is believed to affect neurodevelopment through its direct interaction with the endocannabinoid system. This system is crucial for regulating nerve cell development, migration, connections, and the growth of protective coverings around nerve fibers, as well as the development of neurotransmitter systems. Therefore, cannabis exposure during brain development, whether in early life (prenatal or childhood) or adolescence, has the potential to alter the endocannabinoid system. Such exposure could impact the development of neural pathways involved in reward, emotional regulation, and various cognitive abilities like executive functioning, decision-making, learning, abstract thinking, and attention—all processes central to substance use disorders and other psychiatric conditions.

There are growing concerns that adolescent-onset cannabis use is linked to an increased occurrence and severity of mental health disorders, including psychosis, depression, anxiety, bipolar disorder, and other substance use disorders. Youth who use cannabis are also more likely to report suicidal behavior, including suicide attempts. Among the various mental health challenges, significant attention has been paid to the co-occurrence of cannabis use and psychosis. Although debates continue regarding their direct cause-and-effect relationship, research highlights cannabis use factors such as frequency, potency, and earlier age of onset as risk factors for psychosis. Additionally, a recent study of over 6 million individuals in Denmark showed that CUD was a major risk factor for schizophrenia, especially among young males. While the study could not establish direct causation or conclude that CUD is a modifiable risk factor, the authors estimated that preventing CUD could potentially prevent as many as 30% of schizophrenia cases among men aged 21–30 years. The relationship between cannabis use and mental health is likely bidirectional, with shared predisposing risk factors, brain changes, and overlapping genetics that may contribute to high rates of co-occurring conditions.

Cannabis Use Disorder Risk

Beyond co-occurring psychiatric conditions, several risk factors for developing CUD have been identified, including social factors, environmental conditions, and personality traits. However, large-scale studies consistently point to two primary factors associated with CUD risk. The first is age, specifically for both the initial use and the frequency of use at a younger age. Similar to many other psychiatric conditions, the risk of CUD peaks during adolescence, with most cases becoming apparent between ages 18–30 years. Individuals who begin using cannabis before age 16 are at the highest risk of developing CUD. Furthermore, youth who start using before age 18 are significantly more likely to develop CUD, experience continued substance-related problems into adulthood, and face adverse psychiatric and personal outcomes. The risk of developing CUD also increases significantly among youth who use cannabis at least weekly, with the highest prevalence among those who use it daily. One large study reported that increased use frequency was associated with an 8 to 17-fold increased risk for developing CUD.

The heightened vulnerability to CUD following early cannabis use is thought to involve developmental changes in specific brain regions that control reward, emotion processing, and cognitive control. Long-term brain imaging studies from a European consortium tracking teenagers from age 14 showed that adolescent cannabis use is linked to accelerated thinning of the brain's outer layer (cortex), which was also correlated with impulsive behavior. This finding of cortical thinning aligns with several cross-sectional brain imaging studies. Additionally, the activity of the amygdala, a brain region involved in emotion, during adolescence can predict future cannabis use and CUD. Brain imaging studies in adults diagnosed with CUD also report similar changes in these reward and emotion-related brain areas. More recent and ongoing long-term brain imaging efforts include the Adolescent Brain Cognitive Development (ABCD) study, which has tracked youth from ages 9–10 years. Emerging data from this study suggest that early initiation of cannabis use and CUD are predicted by early childhood adversity, early use of tobacco and alcohol, and maternal prenatal cannabis use. However, establishing the exact cause-and-effect relationship between these factors and cannabis use remains challenging.

The second factor consistently associated with CUD risk is biological sex. CUD rates are typically higher among males, but notable sex differences exist in use patterns, motivations, and CUD presentation. For instance, males are more frequently diagnosed with CUD and show higher rates of use. However, when controlling for how often cannabis is used, the incidence of CUD does not differ between sexes. Females often show a faster progression to CUD, a phenomenon known as "telescoping." Similarly, females with CUD may be more likely to experience increased withdrawal symptoms, co-occurring anxiety or mood disorders, and interpersonal difficulties. These data suggest that cannabis and certain products may have different subjective and physiological effects in males and females, which could ultimately influence CUD development. Importantly, the disparity in CUD rates between sexes is narrowing, possibly due to higher consumption by young females or the increasing potency of products used today.

A Changing Product and Use Pattern in the Cannabis Landscape

The commercialization of cannabis products in legal markets has led to a sharp increase in THC potency, as well as the availability and use of high-THC products like dab pens, wax, or shatter among youth. While recent studies suggest that high THC potency may increase the risk of developing CUD, the impact of using current THC concentrates on adolescent brain development remains largely unstudied. To date, integrating research findings has also been difficult due to varied and inconsistent measures of exposure. This is partly because of the wide array of cannabis products, with many individuals regularly using more than one type. Furthermore, very little information is known about the type of cannabis and cannabinoid products being used, including recently identified rare but extremely potent cannabinoids like tetrahydrocannabiphorol (THC-P), which are now widely available commercially. Information is also lacking regarding the spread of hemp-derived products that bypass state and federal laws by chemically converting non-intoxicating cannabidiol into other THC analogs (e.g., Δ8-THC, Δ10-THC, and hexahydrocannabinol [HHC]). The same challenges apply to precursor products like THC-acid (THCA), which converts to Δ9-THC when heated. Although adolescents and young adults often believe these popular new THC analogs are "healthier," they can produce effects similar to or even stronger than Δ9-THC. The mental health implications of these new THC analogs require significant monitoring and research.

Another crucial factor for CUD is the developmental pattern of cannabis use relevant to its severity. Most studies that track how often cannabis is used ask about prevalence within a specific timeframe, usually the past 30 days, past year, or lifetime. As mentioned earlier, the frequency of cannabis use is linked to an increased risk of developing CUD, but some clinicians mistakenly use frequency alone as a measure of CUD severity. Considering factors used to identify alcohol use disorder might offer new insights into high-risk patterns of cannabis use and CUD development. For example, cannabis use in the morning (e.g., as an "eye opener" or "wake and bake") may indicate more problematic use. However, such information is often not included in current CUD screening and diagnostic tools. Similarly, patterns of heavy, episodic cannabis use (binge use) have not been well-defined, and the impact of consuming large amounts of high-potency THC episodically on CUD development is unknown. Alternatively, a better understanding of an individual’s use beyond simple timeline recall could be achieved by more widely adopting subjective measures of cannabis use, although further studies are needed to validate these measures and establish a consensus for future research guidelines.

Insights from Preclinical Models

Multidisciplinary efforts are essential to address the critical need to understand how the growing diversity of cannabis and cannabinoid products impacts brain development. Animal models therefore remain a vital resource for investigating the causal effects of cannabinoids on the developing brain that may be relevant to the origin of CUD. Preclinical studies to date have provided unique insights, showing that prenatal and adolescent THC exposure increases anxiety-like behavior, deficits in social interaction, increased depression-like behavior, vulnerability to addiction, and cognitive deficits. These deficits are linked to changes in specific brain regions (like the prefrontal cortex, nucleus accumbens, and amygdala), gene expression, protein levels, and cell structure. For example, rodent models of adolescent THC exposure show reduced structural complexity of certain brain cells (pyramidal cortical neurons), which aligns with the cortical thinning observed in human adolescent studies. These animal models have also clarified the unique biological mechanisms in the brain associated with high-potency THC use during adolescence and its impact on brain and cognitive behaviors relevant to CUD risk.

However, there are still significant gaps in translating findings from existing animal models to the current human cannabis landscape. For example, most preclinical studies use injections to administer cannabinoids and determine their impact on behavior, physiology, and molecular changes. This is partly because rodents do not easily self-administer THC through traditional intravenous "addiction" methods and often find THC unpleasant. Although THC injections have revealed important relationships between the drug and its outcomes, human users primarily smoke, vape, or consume edible cannabis products. New data from rodent studies indicate that vaporized THC produces different peak levels in the blood and brain, different metabolic profiles, and different molecular and behavioral outcomes compared to injected THC. Furthermore, rats will self-administer vaporized cannabis extracts, and adolescent animals will voluntarily consume edible THC in gelatin. These new translational models create opportunities to better understand how cannabis exposure and self-administration during development impact the trajectory of brain processes and behaviors relevant to CUD risk.

To maximize the potential of new translational models, both clinical and preclinical fields need to standardize the metrics for key outcomes. This includes determining fundamental pharmacological measures (e.g., peak plasma concentrations, metabolite profiles) to better compare the impact of potency in animal models versus humans, as well as setting standard, translationally relevant behavioral outcomes that mimic behaviors observed in humans. The integration of long-term study designs should test behaviors across development into adulthood, using doses and administration routes that are relevant to current human cannabis consumption patterns. These preclinical efforts will accelerate our understanding of the mechanisms by which developmental THC and cannabinoids causally influence characteristics relevant to psychiatric and CUD risk.

Addressing Adolescent Cannabis Use

Treatment is another crucial factor in addressing the evolving cannabis landscape. Unfortunately, there is currently a significant gap between the estimated number of youth with CUD and the number who receive evidence-based treatment. Current treatment strategies are limited, primarily consisting of motivational enhancement and cognitive behavioral therapies. Given that the increased potency of cannabis and cannabinoid products is expected to raise CUD risk, it is concerning that less than 10% of youth who meet criteria for a substance use disorder, including CUD, receive treatment. More recently, there has been a decline in CUD treatment admissions among youth across the United States, including in states with recreational marijuana laws.

Even when treatment is available, adolescents often do not engage because they do not perceive a need for it. With the expansion of recreational laws and the legal classification of cannabis as "medicinal" at the state level, the perceived harm of cannabis use continues to decrease. In fact, some studies suggest that youth perceive concentrated THC products, particularly vapes or dab pens, as less harmful than combustible plant-based products. This is further complicated by the belief that cannabis use helps with mental health problems, which may actually be worsened by cannabis use. Broad educational efforts are needed, but educating youth about cannabis is complex due to the vast amount of information and misinformation available online and through social media. Individualized interventions may be more effectively delivered by primary care and mental health professionals, who can also address individual and family factors that often contribute to co-occurring mental health problems.

Challenges also exist in providing treatment. The few evidence-based interventions currently used to treat CUD have limited availability and efficacy. This is coupled with a potential lack of awareness regarding cannabis-related problems. For example, physiological changes consistent with tolerance and withdrawal, which individuals self-report, are often not recognized as problems related to cannabis use. Insufficient clinical screening and unrecognized substance-related problems may also lead clinicians to completely miss problematic cannabis use or inaccurately classify adolescent cannabis use as misuse rather than a CUD. Furthermore, clinicians may not screen for substance use problems due to a lack of available resources or programs to which youth can be referred.

A multifaceted approach is necessary to bridge this gap in care, including broader implementation of universal and selective interventions. The risk and protective factors for the onset of cannabis use in youth can be understood using the socio-ecological model, which suggests that factors at multiple levels—including individual and peer, family, school, and community—contribute to cannabis use. Using this framework, current evidence supports the widespread implementation of universal and selective interventions that enhance protective factors and reduce risk factors. This could involve implementing evidence-based interventions at the institutional (e.g., school) or community level. Integrating behavioral interventions into primary care, social work, and school-based settings offers a significant opportunity to leverage existing infrastructure and provide treatment where youth are already engaged in other services. Moreover, as states compete to use tax revenue from the growing cannabis industry, a substantial portion of these funds must be allocated to early intervention and prevention strategies to lessen the impact of cannabis on the developing brain.

Conclusions

The relationship between developmental cannabis use, the impact of high-potency products, and the increased risk of developing CUD and mental health problems must be taken seriously, particularly in light of the current mental health crisis. The developing brain's plasticity offers crucial opportunities for prevention and early intervention to change these trajectories. Clearly, new treatment strategies are needed to address the growing challenge of CUD risk in teenagers and young adults. While data accumulated over past decades about the effects of what are now considered “low dose” THC products have been valuable, significant research efforts in preclinical models are needed, focusing on THC potency relevant to today’s products. Additionally, long-term studies, such as the ABCD study, should provide important insights about factors related to resilience that may also help guide the development of intervention strategies. Altogether, combined long-term, clinical, and preclinical efforts will provide unprecedented knowledge to mitigate the course of CUD and related psychiatric disorders, both of which have strong roots in neurodevelopment.

Adolescent Cannabis Use

In 2022, about 38% of 12th-grade students in the United States had used cannabis at some point in their lives. This was a 17% increase compared to 1992. While cannabis use among youth aged 12–17 stayed somewhat stable over the last ten years, rates continued to rise for young adults aged 18–25. This older age group also had the highest rates of cannabis use. Not everyone who uses cannabis develops a Cannabis Use Disorder (CUD), which means continuing to use cannabis despite significant problems it causes. However, many do. There is limited data on how common CUD is in young people, especially data from before many states legalized medical and recreational marijuana. A recent study that combined findings from many youth and adult studies found that among those who used cannabis, 22% met the requirements for CUD. Young adults had the highest rates, with 41.1% of 21-year-olds who used cannabis developing CUD.

Scientists are still actively researching the complex ways cannabis and its compounds affect the body, including their potential medical uses or harmful effects, especially on the developing brain. Cannabis contains over 500 chemicals, but Δ9-tetrahydrocannabinol (THC) is the main compound that causes a high. Most people who use cannabis use products with all parts of the plant, but THC has been linked to negative mental health outcomes. The stronger the THC, the greater the chance of developing CUD and worse mental health issues. THC is thought to affect brain development by directly influencing the endocannabinoid system. This system plays a key role in how brain cells form, move, connect, and become insulated, as well as how brain chemicals develop. Therefore, cannabis exposure during brain development—whether before birth, in childhood, or during adolescence—can change the endocannabinoid system. Such changes could then affect brain connections related to feelings of reward, emotional control, and various thinking skills like problem-solving, decision-making, learning, abstract thought, and attention. All these processes are central to substance use disorders and other mental health conditions.

Growing concerns about cannabis use starting in adolescence are due to its link with more frequent and severe mental health conditions, including psychosis, depression, anxiety, bipolar disorder, and other substance use disorders. Young people who use cannabis are also more likely to engage in suicidal behavior, including suicide attempts. Among the various mental health challenges, much attention has focused on cannabis use and psychosis occurring together. Although there is still debate about whether one causes the other, studies point to factors like how often cannabis is used, its strength, and starting use at a younger age as risks for psychosis. A recent study of over 6 million people in Denmark showed that CUD was a major risk factor for schizophrenia, especially among young men. While the authors of that study could not prove that CUD directly causes schizophrenia or that preventing CUD would prevent schizophrenia, they estimated that up to 30% of schizophrenia cases in men aged 21–30 might be avoided if CUD were prevented. The relationship between cannabis use and mental health likely goes both ways, with shared underlying risk factors, changes in brain biology, and similar genetic influences contributing to high rates of both conditions.

Cannabis Use Disorder Risk

Besides mental health conditions, several other risk factors for CUD have been identified, including social factors, environmental conditions, and personality traits. However, large studies consistently point to two main factors linked to CUD risk. The first is age, specifically starting use at a younger age and using it frequently. Similar to many other mental health conditions, the risk of CUD is highest in adolescence, with most CUD cases appearing between ages 18–30. Those who start using cannabis before age 16 are at the greatest risk of developing CUD. Additionally, young people who begin using before age 18 are much more likely to develop CUD, have substance-related problems that continue into adulthood, and experience negative mental health and personal outcomes. The risk of developing CUD also significantly increases for young people who use cannabis at least weekly, with the highest rates among those who use it daily. One large study found that increased frequency of use was linked to an 8–17 times higher risk of developing CUD.

The increased risk for CUD after early cannabis use has been connected to changes in certain brain areas that handle reward, emotions, and thinking control. Long-term brain imaging studies that followed teenagers from age 14 showed that adolescent cannabis use was linked to faster thinning of the brain’s outer layer, which was also connected to impulsive behavior. This finding of brain thinning is consistent with many other brain imaging studies done at a single point in time. Furthermore, how the amygdala (a brain area involved in emotions) responds during adolescence can predict future cannabis use and CUD. Brain imaging studies of adults diagnosed with CUD also show similar changes in these brain areas. More recent long-term brain imaging efforts include the Adolescent Brain Cognitive Development (ABCD) study, which has been tracking young people from ages 9–10. Early data from this study suggests that starting cannabis use and developing CUD early is predicted by difficult experiences in early childhood, starting tobacco and alcohol use early, and a mother's cannabis use during pregnancy. However, it remains challenging to prove a direct cause-and-effect link between these factors and cannabis use.

The second factor consistently linked to CUD risk is biological sex. CUD rates are typically higher among males, but clear differences exist in how genders use cannabis, why they use it, and how CUD appears. For example, males are more often diagnosed with CUD and tend to use cannabis more frequently. However, when comparing people who use it equally often, the number of new CUD cases does not differ between genders. Females show a faster progression to CUD, known as "telescoping." Similarly, females with CUD may experience more severe withdrawal symptoms, have more co-occurring anxiety or mood disorders, and face more relationship difficulties. This information suggests that cannabis and certain products may affect males and females differently, both in how they feel and how their bodies react, which ultimately may influence CUD development. Importantly, the gap in CUD rates between males and females is getting smaller. This could be due to higher consumption by young females or the use of stronger products today.

A Changing Product and Use Pattern in the Cannabis Landscape

The commercial sale of cannabis products in legal markets has led to a sharp increase in THC strength, as well as more availability and use of strong THC products like vape pens, wax, or shatter among young people. While recent studies have shown that high THC strength may be linked to an increased risk of CUD, the effect of using today’s strong THC concentrates during adolescence on brain development has not been studied enough. So far, combining research findings has also been difficult because of various and inconsistent ways of measuring exposure. This is partly due to the wide range of cannabis products available, with many people regularly using more than one type. Also, very little is known about the specific types of cannabis and cannabis compounds being used, including a recently identified but extremely strong compound, tetrahydrocannabiphorol (THC-P), which is now widely available for sale. Information is also lacking about the rapid spread of hemp-derived products that bypass state and federal laws. These products create compounds like Delta-8 THC and other THC analogs (e.g., Delta-10 THC and hexahydrocannabinol [HHC]) by chemically converting cannabidiol, a non-intoxicating compound. The same challenges exist with products like THC-acid (THCA) which turns into standard THC when heated. Although adolescents and young adults often believe these popular new THC-like compounds are “healthier,” they can produce effects similar to or stronger than standard THC. The mental health effects expected from these new THC analogs need significant monitoring and research attention.

Another important factor for CUD is how patterns of cannabis use change over time and relate to how severe the use is. Most population studies ask about cannabis use over a specific period, such as the last 30 days, the past year, or a person’s lifetime. As mentioned earlier, the frequency of cannabis use is linked to an increased risk of developing CUD, but some doctors wrongly use how often someone uses it as a measure of CUD severity. Looking at factors used to identify alcohol use disorder might offer new insights into high-risk cannabis use patterns and CUD development. For instance, using cannabis in the morning (e.g., as an “eye opener” or “wake and bake”) might be a stronger sign of problematic use. However, such information is often not included in current ways of screening for and diagnosing CUD. Similarly, patterns of heavy, short-term cannabis use (binge use) have not been clearly defined, and the effect of occasionally consuming large amounts of strong THC on CUD development is unknown. Alternatively, a better understanding of a person’s cannabis use beyond simply asking about timelines might be achieved by more widely adopting personal reports of cannabis use, although more studies are needed to prove these measures are accurate and to agree on standard guidelines for future research.

Insights from Preclinical Models

Cooperation among many different fields is needed to understand the effects of the wide variety of cannabis and cannabinoid products on brain development. Animal models are therefore a critical tool to investigate how cannabis compounds directly affect the developing brain in ways that relate to the start of CUD. Animal studies to date have shown unique insights, demonstrating that THC exposure before birth and during adolescence increases anxiety, social difficulties, depression-like behavior, a higher chance of addiction, and problems with thinking skills. These problems are linked to changes in certain brain areas (like the prefrontal cortex, nucleus accumbens, and amygdala), how genes work, proteins, and the shape of cells. For example, studies in rats and mice exposed to THC during adolescence show that brain cells (pyramidal cortical neurons) have less complex shapes, which matches the brain thinning seen in human adolescent studies. These animal models have also helped explain the unique brain changes linked to strong THC use during adolescence that affect the brain and thinking in ways relevant to CUD risk.

However, there are still big differences between what existing animal models show and how cannabis is used by humans today. For example, most animal studies inject cannabis compounds to see their effect on behavior, body functions, and cells. This is because rats and mice do not easily give themselves THC through typical addiction study methods and often dislike THC. While THC injections have revealed important links between the drug and its effects, human users mainly smoke, vape, or eat cannabis products. New data from rodent studies indicate that vaporized THC leads to different levels of the drug in the blood and brain, different ways the body breaks it down, and different effects on cells and behavior compared to injected THC. Furthermore, rats can give themselves vaporized cannabis extracts, and adolescent animals will willingly eat THC in gelatin. These new animal models that are more like human use create new opportunities to better understand how cannabis exposure during development and self-use affect the changes in brain processes and behavior linked to CUD risk.

To get the most out of these new animal models, both human and animal research fields need to agree on standard ways to measure important results. This includes determining basic measurements of how the drug works (like the highest levels in the blood and how it’s broken down) to better compare the strength of effects in animal models versus humans. It also means setting standard behavioral results in animals that copy what is seen in humans. Long-term study designs should examine behaviors from development into adulthood, using amounts and ways of taking cannabis that match how people use it today. These animal research efforts will speed up our understanding of how THC and other cannabis compounds during development directly influence behaviors and conditions relevant to mental health issues and CUD risk.

Addressing Adolescent Cannabis Use

Another important factor in dealing with the changing cannabis landscape is treatment. Unfortunately, there is a significant gap between the estimated number of young people with CUD and how many actually receive treatment that is proven to work. Current treatment strategies are limited and mainly consist of motivational enhancement and cognitive behavioral therapies (types of counseling). Given that the increased strength of cannabis and cannabinoid products is expected to increase CUD risk, it is concerning that less than 10% of young people who qualify for a substance use disorder, including CUD, receive treatment. More recently, there has been a decrease in young people entering treatment for CUD across the United States, even in states with laws allowing recreational marijuana.

Even when treatment is available, adolescents often do not participate because they do not think they need help. With more states allowing recreational cannabis and classifying it as “medical” by law, the perceived harm of cannabis use continues to decrease. In fact, some studies suggest that young people believe strong THC products, especially vapes or dab pens, are less harmful than smoking plant-based products. This is further complicated by the belief that cannabis use helps with mental health problems, which may actually be made worse by cannabis use. Widespread education efforts are needed, but teaching young people about cannabis is challenging due to the large amount of true and false information available online and on social media. More personalized help might be better delivered by doctors and mental health professionals, who can address individual and family factors that often contribute to co-occurring mental health problems.

Challenges also exist in providing treatment. The few evidence-based treatments currently used for CUD are limited in their availability and how well they work. This is coupled with a potential lack of understanding about cannabis-related problems. For example, physical changes reported by users, like needing more to get the same effect (tolerance) and feeling sick when stopping (withdrawal), are often not recognized as problems related to cannabis use. Insufficient checks by doctors and unidentified substance-related problems may also lead to doctors missing problematic cannabis use entirely or wrongly labeling adolescent cannabis use as just “misuse” instead of a CUD. Furthermore, doctors may not screen for substance use problems due to a lack of available resources or programs to which young people can be sent for help.

A plan with many different parts is needed to address this lack of care, including more widespread use of prevention programs for everyone and for specific at-risk groups. Factors that increase or decrease the chance of young people starting cannabis use can be understood using the socio-ecological model. This model suggests that influences from different areas—like a person’s individual choices, friends, family, school, and community—all play a role in cannabis use. Using this approach, current research supports widespread use of programs that build strengths and lower risks. This may include putting proven programs into action at the institutional (e.g., school) or community level. Adding behavioral help into places like doctor’s offices, social work programs, and schools presents a significant opportunity to use existing systems and provide treatment where young people are already getting other services. Moreover, as states compete to use tax money from the growing cannabis industry, a large portion of these funds must be used for early help and prevention strategies to lessen cannabis’s effect on the developing brain.

Conclusions

The relationship between cannabis use during development, the effects of strong products, and the increased risk of developing CUD and mental health problems must be taken seriously, especially given the current mental health crisis. The brain’s ability to change during development offers chances for prevention and early help to alter the course of these problems. Clearly, new treatment strategies are needed to address the growing challenge of CUD risk in teenagers and young adults. While information gathered over past decades about the effects of what is now considered “low-dose” THC has been very valuable, significant research efforts using animal models are needed, focusing on THC strength like what is found in today’s products. Additionally, long-term studies such as the ABCD study should provide important insights into factors that help people cope and recover, which may also help guide the creation of helpful programs. Overall, combining long-term studies, observations from doctors, and animal research will provide new knowledge to reduce the course of CUD and related mental health problems, both of which are strongly linked to brain development.

Adolescent Cannabis Use

More young people are using cannabis. In 2022, about 38 out of 100 students in 12th grade had used cannabis at some point. This is more than in 1992. Use has stayed about the same for those aged 12 to 17. But more young adults, aged 18 to 25, are using it. This older group uses cannabis the most. Not everyone who uses cannabis will have a problem with it. But many do. This problem is called Cannabis Use Disorder (CUD). It means a person keeps using cannabis even when it causes big problems in their life. Studies show that about 22 out of 100 people who use cannabis develop CUD. This problem is most common in young adults, especially around age 21. For them, about 41 out of 100 cannabis users develop CUD.

Scientists are still learning how cannabis affects the growing brain. Cannabis has over 500 chemicals. THC is the main chemical that makes a person feel "high." Most people use cannabis products that have many of these chemicals. But THC alone can cause problems with a person's mind. The more THC in a product, the higher the chance of getting CUD and having worse mental health. THC can change how the brain develops. This is because THC affects a system in the brain called the endocannabinoid system. This system helps the brain grow and connect properly. If a young person uses cannabis while their brain is still growing, it can change this system. This can affect how the brain handles feelings, makes choices, learns, and pays attention. These brain changes can lead to problems like CUD or other mental health issues.

Using cannabis as a young person can lead to more and worse mental health problems. These include problems like seeing or hearing things that are not there (psychosis), sadness (depression), worry (anxiety), and sudden mood changes (bipolar disorder). Young people who use cannabis may also be more likely to try to harm themselves. A lot of focus is on cannabis use and psychosis. Scientists are still trying to understand if one causes the other. But using cannabis often, using strong cannabis, or starting to use it at a younger age can increase the risk of psychosis. One study in Denmark found that CUD was a big risk factor for a serious mental illness called schizophrenia, especially for young men. The study thought that stopping CUD could prevent many cases of schizophrenia in young men. It is likely that cannabis use and mental health problems can affect each other, and they might share common reasons why they happen.

Cannabis Use Disorder Risk

Besides other mental health problems, some things make it more likely for a person to develop CUD. These include things like a person's friends, their home life, or their personality. But two main things stand out from large studies. The first is age. Starting to use cannabis at a younger age, and using it often, increases the risk. The risk for CUD is highest during the teen years and young adulthood (18-30 years old). People who start using cannabis before age 16 have the highest risk of CUD. If young people start before age 18, they are much more likely to have ongoing problems with cannabis into adulthood. They may also have other mental health problems and personal issues. The risk of CUD also goes up a lot if a young person uses cannabis at least once a week. The highest risk is for those who use it every day. One big study found that using cannabis often made the risk of CUD 8 to 17 times higher.

When young people start using cannabis early, it can harm parts of the brain that handle rewards, feelings, and self-control. Brain scans of teens show that using cannabis can make parts of the brain thinner. This thinning is linked to acting without thinking. Other studies also show these brain changes. Studies also show that how a part of the brain called the amygdala reacts in teens can predict cannabis use and CUD. Newer studies, like the ABCD study, are watching young people from age 9 or 10. They are finding that starting cannabis use early and getting CUD can be linked to hard times in early childhood, starting tobacco and alcohol early, and a mother using cannabis while pregnant. But it is still hard to say if these things directly cause cannabis use.

The second main thing that affects CUD risk is being male or female. Usually, more males are found to have CUD, and they use cannabis more often. But if males and females use cannabis the same amount, the chance of getting CUD is similar for both. Females often get CUD faster after they start using. Also, females with CUD might have worse withdrawal signs, more problems with worry or sad moods, and more trouble with other people. This suggests cannabis might affect males and females differently. It is important to know that the difference in CUD rates between males and females is getting smaller. This could be because more young females are using cannabis, or because today's cannabis products are much stronger.

A Changing Product and Use Pattern in the Cannabis Landscape

With cannabis being sold legally, products now have a lot more THC in them. Stronger products like dab pens and wax are easy for young people to get and use. Studies show that very strong THC can raise the risk of CUD. But we do not know enough about how these super-strong products affect a teen's growing brain. It is hard for studies to keep up because there are so many different cannabis products, and many people use more than one type. There are also new, very strong chemicals in cannabis products, like THC-P, that are now sold widely. Plus, new products made from hemp, like Delta-8 THC, are sold even though they might not follow all laws. Young people often think these new products are safer, but they can have effects like or even stronger than regular THC. We need a lot more study and care to understand how these new products affect mental health.

How a person uses cannabis also matters for CUD. Studies often ask how often someone used cannabis in the last month or year. Using cannabis often increases the risk of CUD, as said before. But just how often someone uses it does not always tell how serious their problem is. We can learn from how we identify alcohol problems. For example, using cannabis first thing in the morning might show a problem. But doctors do not always look for this kind of information when checking for CUD. We also do not know much about "binge" cannabis use, which means using a lot of strong THC at once. We need more study on how this affects CUD. We also need better ways to understand how people use cannabis beyond just how often.

Insights from Preclinical Models

Many types of scientists need to work together to understand how all the different cannabis products affect the growing brain. Studies using animals are very important for this. They help us learn how cannabis chemicals truly affect a young brain and could lead to CUD. So far, animal studies show that being around THC before birth or as a teen can cause more worry, trouble with friends, sad feelings, a higher chance of addiction, and problems with thinking. These problems are linked to changes in important brain areas. For example, animal studies show that teens exposed to THC have fewer connections in brain cells. This matches how human studies show the brain's outer layer getting thinner. Animal studies also help us understand how strong THC affects a teen's brain and thinking, which can raise the risk of CUD.

There is still a big gap between animal studies and how people actually use cannabis today. Most animal studies give cannabis chemicals through shots. This is because it is hard to get animals to take THC on their own, and they often do not like it. Giving shots has taught us a lot, but people usually smoke, vape, or eat cannabis. New animal studies show that vaping THC changes how much THC is in the blood and brain, and how the body breaks it down. This leads to different effects than from shots. Also, now we can get rats and young animals to vape cannabis or eat THC in a gel. These new ways of studying help us better understand how using cannabis as a young person affects the brain and actions, which is important for CUD risk.

To make these new animal studies most helpful, scientists who work with people and scientists who work with animals need to agree on how to measure things. This means finding out how much cannabis chemical is in the body and how it is broken down. This helps compare how strong cannabis affects animals versus people. It also means setting up standard ways to test how animals act, so it matches what we see in people. Studies should also follow animals over a long time, into adulthood. They should use amounts and ways of giving cannabis that are like what people use today. These animal studies will quickly help us understand how THC and cannabis chemicals cause mental health problems and raise the risk for CUD in young people.

Addressing Adolescent Cannabis Use

It is very important to get help for young people who have problems with cannabis. Many young people have CUD, but not enough of them get the right kind of help. The ways we treat CUD now are few. They mainly include talking to someone to help them want to change and learning new ways to think and act. Cannabis products are getting stronger, which means more young people might get CUD. It is concerning that fewer than 10 out of 100 young people who need help for CUD actually get it. Also, fewer young people are going into treatment for CUD across the country, even in places where cannabis is legal.

Even when help is there, teens often do not use it because they do not think they need it. As more places make cannabis legal, and say it is for medicine, young people think it is less harmful. Some studies even show that young people think strong products like vapes are less harmful than smoking cannabis. It is also hard because some young people think cannabis helps with mental health problems, even though it can make them worse. We need to teach more about cannabis, but there is so much true and false information online. It might be better for doctors and mental health helpers to talk to young people and their families one-on-one. They can help with personal and family issues that often go along with mental health problems.

There are also problems with giving treatment. The good treatments we have for CUD are not easy to find, and they do not always work for everyone. People might not understand that they have a problem with cannabis. For example, they might not see that needing more cannabis to get the same effect, or feeling sick when they stop, are signs of a problem. Doctors might not ask enough about cannabis use, or they might not see a serious problem. Sometimes, doctors do not check for drug problems because they do not know where to send young people for help.

We need many different ways to fix this gap in care. We need to offer help to all young people, and also special help to those who are at higher risk. Young people start using cannabis for many reasons, including what happens with their friends, family, school, and community. We should use this idea to help young people. We need to offer programs that make good things stronger and lower the risks. This means putting good programs in places like schools or in the community. We should also add these help programs into doctor's offices, social worker's offices, and schools, where young people already go. Also, as states make money from selling cannabis, a lot of that money should go to programs that help young people early on and prevent them from using cannabis. This will help protect their growing brains.

Conclusions

We must take serious notice of how cannabis use, especially strong products, affects young people's growing brains. It raises the risk for CUD and mental health problems. This is very important given how many mental health problems young people are facing today. A young brain can change, so we have a chance to prevent problems or help early on. We clearly need new ways to treat CUD in teens and young adults. Studies from past years about weaker THC were helpful, but we need more research, especially using animal models, to study today's very strong THC products. Also, long-term studies like ABCD can give us important clues about what helps young people be strong and healthy. This will help us create new ways to help. All these studies together will give us important new knowledge to stop CUD and other mental health problems that start when the brain is developing.