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Published: 22 July 2026

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PMID: 41801216 . DOI: 10.1001/jamainternmed.2025.8215

Abstract

Importance: Cannabis use is common among those with mental health conditions, and many people report using cannabis to manage mental health symptoms. It is important for clinicians to understand the lack of clear benefits of cannabis for mental health conditions and the potential for substantial adverse effects.

Observations: Overall, the potential benefits of cannabis for mental health conditions remain poorly studied. There is low-certainty evidence that Δ-9-tetrahydrocannabinol (THC)-predominant cannabis may not improve symptoms of posttraumatic stress disorder, and there is largely insufficient evidence to characterize the effects of long-term THC-predominant cannabis use on anxiety, depression, and attention-deficit/hyperactivity disorder. There is emerging low-certainty evidence that the cannabis constituent cannabidiol alone may reduce anxiety in patients with anxiety disorders. THC-predominant cannabis use holds substantial risk for adverse mental health effects, and counselling patients about these risks is crucial to promote safety. These risks include worsening mania symptoms and function in those with bipolar disorder and an increase in psychotic symptoms in those with psychotic spectrum disorders. Among people with past-year cannabis use, about 3 in 10 have cannabis use disorder (CUD), and about one-half those with CUD have moderate or severe disease with negative social, employment, or other adverse outcomes. Regular use of high THC-content products by adolescents and young adults is associated with several concerning risks, including an increased risk of psychosis (estimates range from about 2-fold to 11-fold increased risk), a higher risk of CUD, and self-harm in those with mood disorders. Cannabis use should be avoided in individuals at elevated risk of harms, including adolescents and young adults, those with bipolar or psychotic disorders, pregnant individuals, and those at risk for substance use disorders.

Conclusions and relevance: The current evidence base is not sufficient to support the use of cannabis for the treatment of mental health conditions and demonstrates substantial risks of adverse effects. Clinicians should engage patients with mental health conditions in discussions about cannabis use because use is common, has an influence on mental health symptoms, and is likely an important modifiable risk factor for mental health conditions in some populations.

(Complete Research: Cannabis and Mental Health: A Review - PubMed)

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Published: 21 July 2026

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Every year, another cohort of teenagers reaches the age where cannabis becomes available to them: through a dealer, a friend, or increasingly, a legal dispensary. Most try it once or twice and move on. A smaller group use it regularly through adolescence. Experts have argued for decades over what that regular use does to a brain still under construction, usually in terms that generate more heat than light. A study published in February 2026 in JAMA Health Forum does not end that argument, but it does move the conversation about cannabis and the adolescent mind onto firmer ground. It puts a number on the risk, using one of the largest and most carefully built datasets on the subject to date, and it is worth walking through in some detail, because the strength of its conclusions rests on how researchers built it.

A Cohort Built for This Question

Researchers at Kaiser Permanente Northern California, an integrated health system covering more than 4.6 million members, tracked 463,396 adolescents aged 13 to 17 who had completed a confidential screening questionnaire during routine well-child visits between 2016 and 2023. Every teenager in the system answered the same question at each biennial check-up: did you use marijuana in the past year? Researchers recorded that answer as a time-varying exposure, meaning it could change from one visit to the next as a teenager’s habits changed, rather than staying fixed at a single point in time. They then followed adolescents forward through their electronic health records, in some cases as far as age 26, and pulled any subsequent diagnosis of a psychotic, bipolar, depressive, or anxiety disorder from clinical coding rather than a symptom survey. That distinction matters. This was not a study asking teenagers to rate how anxious they felt. It was tracking who actually walked into a doctor’s office and received a formal diagnosis.

The scale of the cohort lets the study do things smaller studies cannot. Of the 463,396 adolescents, just over half were male, the average age at enrolment was 14.5, and the sample was ethnically broad: 29.5 percent Hispanic, 20.2 percent non-Hispanic Asian, 7.6 percent non-Hispanic Black, 33.0 percent non-Hispanic White, and 4.1 percent multiracial or of other backgrounds. At baseline, 5.7 percent of adolescents, 26,345 teenagers, reported past-year cannabis use. That group looked demographically different from their non-using peers. Cannabis users were older on average, more likely to be Hispanic, non-Hispanic Black, or non-Hispanic White, and less likely to be non-Hispanic Asian. They were also more likely to be on Medicaid, to live in more deprived neighbourhoods, and to report drinking alcohol or using other substances, nearly two-thirds of cannabis-using teenagers also reported drinking, compared with just over three percent of non-users. This pattern of overlapping risk is exactly why the researchers built their statistical models to adjust for all of it: sex, race and ethnicity, neighbourhood deprivation, insurance type, and alcohol and other drug use, all entered as covariates rather than left to confound the picture.

Doubled Risk of Psychosis and Bipolar Disorder

Over the follow-up period, the cohort generated 4,105 new diagnoses of psychotic disorder, 4,061 of bipolar disorder, 62,137 of depressive disorder, and 73,096 of anxiety disorder. Psychosis and bipolar disorder were, in absolute terms, rare: around a quarter of a case per thousand person-years each. Depression and anxiety were far more common, at four to six cases per hundred person-years. Set against cannabis exposure, the pattern was consistent across all four. Adolescents who reported past-year cannabis use were 2.19 times more likely than non-users to receive a psychotic disorder diagnosis and 2.01 times more likely to receive a bipolar disorder diagnosis, after the researchers adjusted for the full set of covariates. The links to depression and anxiety were smaller in size but still statistically solid: a 1.34-fold increase in risk for depressive disorder and a 1.24-fold increase for anxiety disorder.

These are adjusted figures: the models already account for the more obvious alternative explanations, drinking, other drug use, socioeconomic disadvantage, and none of them explain the pattern away. The researchers then pushed harder, testing whether teenagers who already showed signs of mental illness before using cannabis were simply more likely to do both: use the drug and later receive a diagnosis, for reasons that had nothing to do with cannabis itself. So they reran the models adjusting for each adolescent’s psychiatric history at baseline, and again after removing anyone with any psychiatric history at all, leaving only a cleaner, lower-risk group. Neither check changed the story much. The risk of psychosis and bipolar disorder stayed roughly doubled in both versions (psychosis: 1.92 and 1.99; bipolar disorder: 1.73 and 2.00), and depression and anxiety held in much the same range as the main result (depression: 1.33 and 1.37; anxiety: 1.19 and 1.22). Whichever way the researchers sliced the data, the pattern survived.

They also checked whether their definition of psychosis was doing too much work. Clinicians coded roughly two-thirds of the psychotic disorder diagnoses in the cohort as unspecified psychosis rather than a named condition like schizophrenia, so the researchers tried both a broader definition, one that also captured substance-induced psychosis, and a narrower one limited to unspecified psychosis with no drug involvement coded. Both versions landed almost exactly where the main finding did, around a doubling of risk (2.20 with the broader definition, 2.21 with the narrower one). The result wasn’t an artefact of how the researchers happened to define psychosis.

Correlation, Causation, and Timing

None of this proves cannabis causes these disorders the way smoking causes lung cancer. What a cohort study can show is sequence: cannabis use came first, and reliably so. Among adolescents who went on to receive a diagnosis, the average gap between first reporting cannabis use and receiving a psychiatric diagnosis ranged from 1.7 years for depressive disorder to 2.3 years for bipolar disorder. That is not proof of causation, but it rules out the simplest alternative explanation, that the diagnosis came first and the cannabis use was somehow a consequence of it, at least for the majority of cases captured in the data.

What the study cannot fully rule out is that something else entirely, a genetic vulnerability, an adverse childhood experience, an undiagnosed mood problem already forming beneath the surface, is driving both the cannabis use and the later diagnosis simultaneously. Statisticians have a tool for stress-testing exactly this worry, called an E-value. It asks a simple question: how powerful would a hidden factor have to be, in its own effect on both cannabis use and the outcome, to erase the association entirely? A low number means a fairly ordinary confounder could do the job, and readers should treat the finding cautiously. A high number means the hidden factor would have to be doing something dramatic, which makes coincidence a less comfortable explanation. Here, the numbers came out high for the two more severe conditions and lower for the others: 3.79 for psychosis and 3.44 for bipolar disorder, meaning a hidden factor would need to nearly quadruple the odds of both cannabis use and the disorder to explain the link away, against 2.02 for depression and a more modest 1.79 for anxiety. That pattern is part of why the psychosis and bipolar findings carry more weight in the paper than the depression and anxiety ones, and part of why this study has become a reference point for anyone examining cannabis and the adolescent mind rather than just another entry in the literature.

Younger Users Carry the Greater Risk

One of the more striking patterns in the data only appeared once the researchers checked whether the strength of the association held steady across age. For depression and anxiety, it did not. The risk tied to cannabis use was highest in early adolescence and steadily faded as the cohort got older, almost like a countdown. For depressive disorder, it started at a 78 percent increase in risk for 13 to 15 year olds and eased with each older bracket until it disappeared entirely by the early twenties, no longer statistically distinguishable from zero (1.78, then 1.35, then 1.21, then a non-significant 0.97). Anxiety traced almost the same arc, starting at a 47 percent increase and fading out by ages 21 to 25 (1.47, then 1.24, then 1.24, then a non-significant 0.95). Psychosis and bipolar disorder did not follow this pattern. Whatever is driving the elevated risk for those two conditions appears to work differently to whatever links cannabis to depression and anxiety, and it does not fade out simply because the person using cannabis has grown older.

The Endocannabinoid System and a Brain Still Under Construction

The clinical numbers line up with a body of laboratory and neuroimaging research the Dalgarno Institute, an Australian drug policy and prevention body, has been compiling for years, work that has quietly built the biological case for cannabis and the adolescent mind long before the Kaiser Permanente cohort gave it a population-level number to point to. The mechanism centres on the endocannabinoid system, a receptor network deeply involved in how the adolescent brain wires itself, particularly the circuits governing motivation, emotional regulation, and affective processing. THC, cannabis’s main psychoactive compound, acts directly on cannabinoid receptors that are especially dense in the adolescent brain. The Institute’s archive holds translational work, combining human neuroimaging with animal studies, that argues high-THC products can disrupt this developmental process, with effects on emotional regulation that outlast the period of use itself. That literature frequently cites one figure putting the increased risk of adolescent psychotic disorder at over elevenfold for cannabis users, a considerably larger effect than the JAMA Health Forum figure. The two studies used different populations, definitions, and methods, so readers shouldn’t read the numbers side by side as apples to apples. But they point the same way: adolescence as a particularly exposed period, with the size of the effect scaling with the potency of what teenagers are using. That detail is worth sitting with given where the JAMA cohort came from. Northern California’s legal cannabis market has an average THC content in flower products exceeding twenty percent, several times higher than the products that much of the older research in this field studied.

This also helps explain why the psychiatric associations were strongest for psychosis and bipolar disorder rather than depression and anxiety. Researchers think psychotic and bipolar disorders have stronger neurodevelopmental roots, conditions that a disrupted brain circuit can tip into during a sensitive window. Depression and anxiety have a wider range of triggers, many environmental and temporary, which may be part of why their link to cannabis use fades as the brain finishes developing and other life factors take over as the dominant influence. A mechanism that specifically interferes with neurodevelopment would likely leave a bigger and more durable mark on the former than the latter, and that is roughly what both datasets show.

TikTok, Micro Influencers, and the New Pathway to Use

The Kaiser Permanente data collection ended before the current wave of social-media-driven exposure had fully taken hold, so it cannot speak to a more recent question: how cannabis first reaches today’s teenagers. A 2025 analysis that the Dalgarno Institute cites, drawing on JAMA Network Open research tracking more than 7,600 California high school students, found that teenagers who saw cannabis content on platforms like TikTok were substantially more likely to start using cannabis within a year, and far more likely to become dual users of cannabis and e-cigarettes. Exposure through micro influencers, social media personalities with modest followings who read to teenagers as peers rather than advertisers, carried the strongest associations of all, with exposed teenagers showing a markedly higher risk of recent cannabis use. That matters for the mental health picture too: the same research flagged heightened depression risk among dual users specifically, on top of whatever burden multiple substances place on a developing brain. It suggests the exposure landscape driving the next cohort of teenagers into cannabis use looks meaningfully different from the one that shaped the adolescents in the Kaiser Permanente study, more engineered, more peer-coded, and harder for parents to see happening.

What the Data Can’t Tell Us

The Kaiser Permanente cohort measured past-year use, not frequency, potency, or method of consumption, all of which likely matter a great deal and this dataset could not tease apart. Diagnosis also depended on a teenager actually presenting to a doctor and clinicians coding the case correctly, so milder or unrecognised cases of depression or anxiety may not appear in the data at all; the two thirds of psychotic disorder diagnoses that clinicians left as unspecified point to genuine diagnostic caution in adolescent psychiatry rather than a fully resolved clinical picture. The Dalgarno Institute material leans heavily on animal models and smaller clinical samples: useful for establishing mechanism, but no substitute for the statistical power of a half-million-person cohort. Each source covers a gap the other leaves open. Neither would be persuasive alone.

A Case for Taking Adolescence Seriously

Taken together, the evidence suggests adolescence isn’t a neutral backdrop against which cannabis use just happens to occur. It looks more like a period when the brain is unusually responsive, for better or worse, to what’s introduced into it. That is, at its core, what the research on cannabis and the adolescent mind is now converging on. The JAMA Health Forum associations were sizeable, survived repeated attempts to explain them away through confounding, and held up under three separate sensitivity checks and two alternative outcome definitions. Set against a growing mechanistic literature on how THC interacts with a developing endocannabinoid system, and newer evidence on how easily social platforms now engineer that exposure, adolescent cannabis use looks less like a rite of passage and more like a genuine public health question, one worth treating as such.

That’s not an argument about legalisation for adults, which involves a different set of trade-offs. It’s a narrower claim: cannabis and a still-developing brain don’t mix cleanly, and the data now backs that up from more than one direction, in populations as different as a Californian health system’s electronic records and a laboratory studying receptor density in animal models. It points toward earlier screening in routine paediatric care, clearer messaging aimed at parents and teenagers rather than adult consumers, and marketing and packaging rules that take seriously how differently a fifteen-year-old responds to this drug compared with a thirty-five-year-old. (Source: WRD News – Dalgarno Institute)

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Published: 21 July 2026

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For many people, cannabis now sits in the same mental basket as a glass of wine or a herbal sleep aid: familiar, legal in some places, and often marketed as a “natural” way to unwind. But a major new brain‑imaging study of more than 1,000 young adults suggests that heavy cannabis use may quietly weaken one of the mind’s most important tools: working memory.¹

Working memory is the mental “command centre” that helps us keep track of what we’re doing, follow multi‑step instructions and juggle information when we solve problems. It’s what allows a nurse to remember several tasks at once on a busy ward, or a student to hold the steps of a complex equation in mind long enough to solve it. When this system doesn’t fire on all cylinders, everyday life feels fuzzier and more effortful—even if intelligence and long‑term memory seem unchanged. news. ²

Inside the largest cannabis–brain study yet

The new research, published in JAMA Network Open, analysed 1,003 young adults in early adulthood, many of whom had used cannabis at some point in their lives. Participants completed a series of thinking and motor tasks while their brain activity was measured using functional MRI—essentially, a live map of which brain regions “light up” when we think and move.³ 

The scientists were especially interested in two things: cannabis use in the last few days (“recent use”) and how often people had used cannabis over their lifetime (“heavy lifetime use”). Heavy lifetime users in this study were those with very frequent use over the years—often more than 1,000 separate episodes. ⁴

What they found should give regular users pause. Heavy lifetime cannabis use was linked to lower brain activation in key areas of the frontal lobes and insula—the regions responsible for attention, planning, self‑control and decision‑making—when people were asked to perform demanding working‑memory tasks. In simple language: the brains of heavy users had to work harder and still did less when asked to hold and manipulate information. ⁵

Not just “being stoned” – changes that linger

We already know that being high can temporarily slow reaction time, cloud judgement and interfere with coordination. Public health agencies warn that recent cannabis use (within about 24 hours) can affect attention, memory, movement and perception. This new study confirmed that recent use was linked to poorer performance and lower brain activation in working‑memory and motor tasks as well. ⁶

But the more concerning finding is what happened when researchers looked beyond the recent high. Many heavy lifetime users showed weaker working‑memory activation even when they were not acutely intoxicated. That hints at long‑lasting changes in how the brain’s control network functions—changes that seem to build up over years of frequent use. ⁷

Interestingly, not every cognitive task in the study showed large, clear differences. Basic thinking skills looked similar across groups. It was specifically the demanding working‑memory task, and the associated brain activation pattern, that seemed most vulnerable. That’s important, because working memory is the foundation for more complex skills like learning, planning and multi‑tasking. ⁸

How this fits with the wider science

This isn’t the first time researchers have flagged cannabis as more than a harmless relaxant. Long‑term studies following people from adolescence into midlife have found that persistent cannabis use is associated with measurable decline in neuropsychological performance, especially in memory and processing speed. Other imaging studies have reported subtle differences in brain structure and function among heavy users, particularly in regions rich in cannabinoid receptors. ⁹

On the other hand, not all findings are uniformly negative. A recent study of adults using cannabis for medical reasons under self‑directed care found no major changes in brain activation patterns after one year, suggesting that occasional or moderate medical use in older adults may carry different risks than heavy recreational use in younger people. This underlines a key point: dose, age and pattern of use matter. ¹⁰

Taken together, the emerging picture is not one of catastrophe, but of a subtle erosion of mental sharpness in some frequent users—especially those who start young and use often. It’s a slow‑burn effect: less dramatic than overdose or psychosis, but potentially significant over decades of study and work.¹¹

What this means for everyday users

For readers of a health magazine, the practical question is simple: “What does this mean for me or my family?”

A few clear messages stand out from the current evidence:

• Frequency matters: The more often cannabis is used, especially over many years, the higher the chance of persistent changes in working‑memory function.
• Age matters: Brains up to about age 25 are still fine‑tuning the networks involved in self‑control, planning and emotional regulation, and appear more sensitive to interference from substances like cannabis.
• Pattern matters: Heavy, regular use is very different from occasional, light use under medical supervision in older adults.

If you are a parent, these findings suggest that normalising cannabis use in late teens and early twenties could mean your child carries subtle but real cognitive disadvantages into university, apprenticeships and early career. If you are a young adult, it’s worth asking how often you rely on cannabis, and whether that pattern might be trading away some mental agility you’ll wish you had later.

A balanced, informed view

None of this research says that everyone who uses cannabis will suffer dramatic brain damage, nor does it deny that some patients may gain relief from carefully monitored medical use. What it does say, with increasing clarity, is that heavy, long‑term use—especially starting young—is not cognitively neutral.

As cannabis becomes more available and socially accepted, the conversation needs to move beyond simple labels of “safe” or “dangerous.” For a health‑conscious readership, the question is whether the short‑term benefits of relaxation or social bonding are worth the potential long‑term cost to the brain’s command centre.

The latest brain‑scan data offer a caution that fits neatly into a broader wellness mindset: if you value focus, memory and mental flexibility, treating cannabis as an occasional indulgence—rather than a daily habit—is likely the safer choice. (Source: JAMA and WRD News)

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Published: 15 July 2026

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A habit that millions of people consider harmless could be quietly raising the odds of a heart attack. A major new review, published in The American Journal of Medicine, has pulled together years of research on cannabis use and heart attack risk, and the picture it paints is far from reassuring, especially for younger adults who assume their hearts are safe.

Cannabis use has climbed sharply over the past decade. In the United States alone, around 19% of adults, roughly 52.5 million people, reported using cannabis in 2021, more than double the figure from ten years earlier. As legalisation spreads and the drug becomes more socially accepted, doctors say the cardiovascular consequences are only now coming into focus.

A Growing Body of Evidence

The review describes cannabis use and heart attack risk as a genuine and often overlooked clinical concern, particularly among people in their twenties and thirties who have none of the usual warning signs, no high cholesterol, no diabetes, no family history. Case reports and larger population studies have repeatedly found heart attacks occurring in young, apparently healthy cannabis users shortly after they consumed the drug.

Among people already living with heart disease, the numbers are striking. Surveys of cardiac patients found that around 4% use cannabis daily and a further 7.1% use it occasionally. In people with premature atherosclerotic heart disease, meaning heart disease that strikes unusually early in life, cannabis use was reported in up to 12.5% of cases.

Why Cannabis Can Trigger a Heart Attack

The mechanisms behind marijuana and cardiovascular risk are more complicated than most people realise. Smoking or vaping cannabis activates the sympathetic nervous system, pushing up heart rate, blood pressure and the force of each heartbeat. All of this raises the heart’s demand for oxygen at the exact moment the drug is also cutting off its supply.

That happens because cannabis smoke raises levels of carboxyhemoglobin in the blood, a compound that reduces how much oxygen red blood cells can actually carry. The heart is asking for more fuel while receiving less of it, a mismatch that researchers believe helps explain why some users suffer heart attacks despite having clear, undamaged arteries.

On top of that, cannabis appears to trigger coronary vasospasm, a sudden and temporary narrowing of the arteries feeding the heart, along with damage to the delicate lining of blood vessels known as the endothelium. The drug has also been shown to activate platelets, the blood cells responsible for clotting, nudging the body towards a prothrombotic state in which clots form more easily than they should.

Not Everyone Is Affected Equally

Interestingly, not every cannabis user faces the same level of danger, and genetics appear to play a real part in that. Variation in cannabinoid receptors, the docking points cannabis compounds attach to in the body, seems to influence whether the drug’s effects lean towards harm or, in some cases, protection. Differences in how the liver enzyme CYP2C9 breaks down THC, the main psychoactive compound in cannabis, may also explain why some people are far more vulnerable than others to its cardiovascular effects.

A Complication for Heart Patients Already on Treatment

Perhaps the most immediately practical finding concerns patients recovering from a stent procedure, formally known as percutaneous coronary intervention. Data from more than 7.3 million such patients in the United States, gathered between 2004 and 2014, found that 0.4% met the criteria for cannabis misuse. Crucially, those patients were considerably younger than average, 49.5 years old compared with 64.6, and more likely to be male.

For these patients, the concerns go beyond the heart attack itself. Many are prescribed clopidogrel, a blood thinning drug designed to stop dangerous clots forming inside a newly placed stent. The review notes that cannabidiol, or CBD, blocks an enzyme called CYP2C19 that the body needs to activate clopidogrel properly. In practical terms, cannabis use could quietly undermine one of the very treatments meant to protect a patient’s heart, prompting the review’s authors to suggest doctors consider alternative medications for patients who use cannabis regularly.

The Numbers Behind the Headlines

Large population studies cited in the review found that daily cannabis use is independently linked to a 25% higher risk of heart attack, even after accounting for other lifestyle factors. That figure sits alongside a wider body of evidence connecting frequent use to elevated cardiovascular risk, although the authors are careful to note that not all long term studies agree, and more rigorous, prospective research is still needed to settle some of the more contested questions.

What This Means Going Forward

The authors are not claiming cannabis is uniquely dangerous compared with other substances, but they are pushing for something simple: better awareness. They argue that questions about cannabis use and heart attack risk deserve the same routine attention in clinics that smoking and alcohol already receive, particularly for younger patients who might otherwise be waved through without a second thought.

As legalisation continues to expand and cannabis edges further into the mainstream, understanding marijuana and cardiovascular risk is becoming less of a niche academic interest and more of an everyday clinical reality. For anyone weighing up the risks, the message from this latest research is straightforward. The heart does not necessarily distinguish between a legal habit and a dangerous one, and for some people, the consequences can arrive without warning.

(Source: WRD News)