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On 25 March 2026, the International Academy on the Science and Impact of Cannabis (IASIC) hosted a presentation by Dr Ragy R. Girgis, M.D., M.S., Professor of Clinical Psychiatry at the Columbia University Department of Psychiatry and the New York State Psychiatric Institute. His subject was cannabis and mass shootings, and the findings come from what is now the most comprehensive mass murder repository ever assembled: the Columbia Mass Murder Database.
The database contains more than 2,300 cases of personal-cause mass murder documented worldwide since 1900. It was not built to prove a point. It was built because Dr Girgis and his colleagues decided they wanted to understand, as definitively as possible, what was actually driving mass shootings rather than relying on assumption, media coverage, or politically convenient narratives.
What it is beginning to reveal about cannabis and mass shootings is not comfortable reading.
Building the Database
Before getting to the findings, it is worth understanding what the Columbia Mass Murder Database actually is, because the rigour of the methodology is what gives the results their weight.
Dr Girgis and his team began by reviewing popular databases of mass murder including Wikipedia, the Stanford database, Mother Jones, Everytown, and others. From those sources they identified potential cases, then excluded anything that did not meet their strict criteria: events had to involve three or more fatalities not including the perpetrator, had to be perpetrated for personal reasons rather than war, terrorism, gang activity or organised crime, and had to be supported by primary sources in English, meaning court and police records or reliable news media rather than secondary websites.
What remained was a dataset of around 1,700 mass murders in the original iteration, now grown to more than 2,300 cases through to 2023 or 2024. It is the largest such dataset in the world.
One of the key design decisions was the use of comparison groups. Most prior research on mass shootings had not included them, which introduced significant bias into the findings. Dr Girgis’s team divided the sample into perpetrators who used firearms and perpetrators who used other methods, on the basis that weapon choice was the most meaningful differentiator between types of mass murder. That comparison structure is what makes the cannabis findings meaningful rather than merely suggestive.
What Most People Get Wrong About Mass Shootings
Before arriving at the cannabis data, Dr Girgis walked through some findings that challenge widely held assumptions.
The first concerns mental illness. Most violence, and most mass shootings, is committed by people without psychotic illness. This is consistent with what the research has long suggested, but it continues to be misrepresented in public debate. Mental illness, specifically psychosis, accounts for roughly 5% of the contributing factors to mass shootings. It is a slice of the pie, not the whole thing.
The second concerns the types of mass shooting people tend to think about. School shootings, which dominate news coverage and public imagination, represent only about 13% of all mass shootings. The most common type, accounting for around 45% of cases, is familicide: mass murder involving a spouse, children, or other family members. The second most common is felony-related mass murder. The public-facing, stranger-targeted mass shooting is actually the least common category, though it attracts the most attention.
The third concerns alcohol. Despite a widespread cultural assumption that alcohol and violence go hand in hand, alcohol misuse showed no meaningful relationship with mass murder in the data. The signal in the data is not about alcohol. It is almost entirely about cannabis.
The Number That Should Prompt Questions
Here is what the data on cannabis and mass shootings actually shows.
In the United States, the prevalence of cannabis involvement among mass shooters before 1996 was around 5%. After 1996, the year medical cannabis was first legalised in California, that figure more than doubled to over 11%. The result was statistically highly significant.
Dr Girgis chose 1996 deliberately, and not arbitrarily. He and his colleagues were aware that using a single date as a policy marker has limitations. So they tested the result using 1990 and 2000 as alternative cutoff years and found the same pattern held. They also noted the well-documented diffusion effect of cannabis laws, whereby legalisation in one state influences use and availability across many others, which further supports the use of a single national date as a meaningful marker.
When the same analysis was applied to perpetrators of mass murder who did not use firearms, there was no increase. No relationship at all. The doubling of cannabis involvement was specific to mass shootings.
That specificity is the most important feature of the finding. It is not simply that cannabis use has increased across the general population since legalisation began, which it has. The relationship shows up specifically in people who used firearms to commit mass murder, and not in a closely comparable group of people who committed mass murder by other means. That is the kind of pattern that, in research terms, begins to suggest something more than coincidence.
Motive, Suicide, and What Cannabis Involvement Tells Us
One of the more revealing findings from the data concerns what cannabis involvement predicts about a perpetrator’s behaviour at the time of the event.
Mass shooters with cannabis involvement were significantly less likely to take their own life at the time of the shooting compared to those without cannabis involvement. To understand why that matters, Dr Girgis explained how researchers think about the barriers that prevent someone from perpetrating a mass murder.
There are three of them. The first is the person’s own moral or value system, whether that is religious, ethical, or psychological in origin. The second is the moral framework they have internalised from the people around them: family, partners, community, society. The third is the rational deterrent of getting caught, prosecuted, and imprisoned.
When a perpetrator plans to die at the scene, that third barrier is removed entirely. It becomes significantly easier, psychologically, to carry out the act. Mass shootings, more than other forms of mass murder, are associated with perpetrators who intend to take their own life, and it is partly for this reason that mass shootings are so much more common than other forms of mass murder involving comparable planning and motivation.
What the cannabis data suggests is that perpetrators with cannabis involvement are operating with a different set of motivations. They are more likely to intend to survive. That changes the profile of the event and potentially the profile of the intervention that might prevent it.
Cannabis involvement was also associated with significantly younger perpetrators. That finding is perhaps less surprising given what is known about cannabis use demographics, but it reinforces the picture of a distinct subgroup of mass shooters for whom cannabis is a meaningful variable.
Correlation, Causation, and What Comes Next
Dr Girgis is precise about the limits of what the data shows. These findings are correlational. Establishing causation would require a randomised clinical trial, which is not feasible in this context. The data cannot tell us that cannabis caused these individuals to commit mass shootings.
What the data can do is establish a specific, statistically significant pattern that is consistent with the broader and well-established body of evidence linking cannabis use and violence more generally. Dr Girgis described that broader evidence as very clear. The relationship between cannabis and violence in general is not contested in the literature. What the Columbia Mass Murder Database adds is a specific examination of that relationship in the context of mass shootings in the United States, with a comparison group designed to account for confounding.
The honest summary is this: cannabis involvement in mass shooters more than doubled after cannabis legalisation began, the relationship is specific to mass shootings rather than mass murder more broadly, and it is consistent with what we already know about cannabis and violence. That is not a finding to dismiss because it is inconvenient.
A Piece of the Pie
Dr Girgis frames the contributing factors to mass shootings as pieces of a pie rather than a single cause. Mental illness accounts for roughly 5%. Recreational drug use, and in this dataset that means almost exclusively cannabis, accounts for another portion. Social, cultural, and situational factors make up the rest.
That framing is important. It resists the temptation to reduce a complex phenomenon to a single explanation, which is exactly what public debate on mass shootings tends to do. After every high-profile shooting, attention immediately focuses on one cause: mental illness, gun laws, social media, school culture. The data suggests the reality is more distributed than that.
But distributed does not mean equal. And a doubling of cannabis involvement among mass shooters following legalisation is not a small signal in a noisy dataset. It is a finding that deserves to be part of the policy conversation.
The Conversation That Keeps Getting Avoided
Cannabis and mass shootings is not a pairing that survives long in public debate. Legalisation is politically popular. The cannabis industry is large and commercially motivated to keep the public narrative positive. And findings like these are easy to dismiss as correlational, preliminary, or simply too uncomfortable to act on.
But the data on cannabis and mass shootings is now emerging from the most rigorous dataset ever applied to this question. Governments expanding cannabis access, and many are, are making long-term decisions about public health without seriously engaging with this research. That is a failure of due diligence dressed up as progress.
Dr Girgis and his colleagues are not campaigners. They are researchers who built a database, applied a comparison structure to control for bias, and reported what they found. That finding is specific: cannabis involvement among mass shooters in the United States more than doubled after legalisation began. It is statistically significant. Moreover, it is consistent with what the broader literature on cannabis and violence already tells us.
The Columbia Mass Murder Database now contains more than 2,300 cases. The pattern around cannabis and mass shootings is clear enough that the question is no longer whether it exists. The question is whether anyone in a position to act on it is paying attention.
Dr Ragy R. Girgis, M.D., M.S., Professor of Clinical Psychiatry, Columbia University Department of Psychiatry and New York State Psychiatric Institute, presented at the IASIC Speaker Series on 25 March 2026. (Source: WRD News)
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A major new study has found that cannabis memory loss goes further than most people expect. Smoking cannabis does not simply blur memories. It can actively distort them, creating false recollections of things that never happened. Washington State University (WSU) researchers say THC, the psychoactive compound in cannabis, disrupts the brain’s ability to store, retrieve, and verify information in ways science is only beginning to map.The team recruited 120 regular cannabis users and tested them across a wide range of memory tasks. The results raise serious questions about everyday cannabis use, particularly as consumption rises sharply across the UK and North America.
Cannabis Memory Loss Is More Widespread Than Previously Thought
Earlier research on cannabis effects on memory tended to focus on simple tasks, such as recalling a list of words. This study went much further. Researchers tested seven distinct types of memory, from remembering future appointments to tracking where information originally came from.
Out of 21 individual memory measures, cannabis intoxication caused significant impairment on 15. That figure alone tells a striking story. Carrie Cuttler, senior author and associate professor of psychology at WSU, says the findings expose just how broad the problem is.
“Most previous studies have only looked at one or two types of memory, like recalling lists of words,” she said. “This is the first study to comprehensively examine many different memory systems at once, and what we found is that acute cannabis intoxication appears to broadly disrupt most of them.”
How Cannabis Effects on Memory Create False Recollections
The strongest impact appeared in false memory. Researchers played participants lists of related words but left out the key connecting word. Later, those who had consumed THC were far more likely to “remember” words that were never actually said, including words with no connection to the list at all.
“I found it was really common for people to come up with words that were never on the list,” said Cuttler. “Sometimes they were related to the theme of the list, and sometimes they were completely unrelated.”
Cannabis memory loss of this kind goes beyond simple forgetting. The brain stops merely failing to record things accurately. It starts generating plausible replacements. That has real consequences, from misremembering conversations to inaccurately reporting what someone witnessed in an incident.
Source Memory: Losing Track of Where Information Came From
Source memory is the ability to remember not just what you know but where you learnt it. Cannabis users in the study struggled to correctly identify the origin of information they had encountered earlier in the session.
This matters because source memory underpins critical thinking. People who cannot reliably recall whether something came from a trusted expert, a rumour, or something they skimmed online grow more vulnerable to accepting false information as true. Researchers noted this has particular relevance in legal settings, where eyewitness reliability is central to the process.
Everyday Cannabis Effects on Memory: Forgetting What You Planned to Do
The study found clear impairment in prospective memory too. This is the ability to remember future tasks. Taking medication on time, attending a meeting, picking something up on the way home, all of these rely on prospective memory.
“These are things we rely on constantly in our day-to-day lives,” said Cuttler. “If you have something you need to remember to do later, you probably don’t want to be high at the time you need to remember to do it.”
For regular cannabis users, these effects could quietly build into a pattern of missed responsibilities and unreliable follow-through.
Even Moderate Doses Produce Significant Disruption
One finding that genuinely surprised the research team was the dose result. Participants who consumed 20 milligrams of THC performed no better than those who consumed 40 milligrams. Both groups showed similarly poor results compared to the placebo group.
That challenges the common assumption that lower doses carry meaningfully lower risk. Even a moderate amount of cannabis appears sufficient to produce broad cognitive disruption in the short term.
Researchers ran the experiment under rigorous double-blind conditions. Neither participants nor the research team knew who had received THC or a placebo until after the study ended.
What the Study Did Not Find
Episodic content memory, the ability to recall personally experienced events, did not show a statistically significant effect. Cuttler cautioned against reading too much into this finding. The team said further research is necessary before drawing firm conclusions in that area.
Growing Use, Growing Concern
Cannabis is now legal for recreational use across much of North America. Use is also rising across parts of Europe. Yet the research into short-term cognitive risks has lagged behind. Cannabis remains a Schedule I substance under US federal law, which limits how it can be studied.
The WSU Health and Cognition (THC) Lab, co-directed by Cuttler and colleague Ryan McLaughlin, works to close that gap.
“We’re living in a state where cannabis use is very common, but there’s still a lot we don’t know about its acute effects,” said Cuttler. “The goal is to help people make informed decisions about the risks and benefits.”
With 15 out of 21 memory measures showing significant impairment, and false memory and source memory among the hardest hit, cannabis effects on memory appear broader and more consequential than many users realise. Cannabis memory loss is not simply a matter of things slipping your mind. It can mean clearly remembering things that never happened at all. (Source: WRD News)
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Impact of Cannabis and Cannabis Legalization on US Atrial Septal Defect Rates
by Albert Stuart Reece & Gary Kenneth Hulse - Division of Psychiatry, University of Western Australia, 35 Stirling Hwy., Crawley, WA 6009, Australia
School of Medical and Health Sciences, Edith Cowan University, 27 Joondalup Dr., Joondalup, WA 6027, Australia
- Xenobiot.2026, 16(2), 43; https://doi.org/10.3390/jox16020043
Abstract
Atrial septal defect (ASD) affects 1:11.3 children in some US states; however, the antecedents of these trends are yet to be identified. A total of 1882 ASD rates (ASDRs) for 2003–2020 were sourced from the National Birth Defects Prevention Network reports. A total of 406,893 ASDs are reported. Substance (cigarettes, binge alcohol, cannabis, cannabinoids, analgesics, cocaine) exposure data were taken from the National Survey of Drug Use and Health. Income and ethnicity data were derived from the US Census. Adjustment was performed by mixed effects, survey and generalized additive regression. Causal analysis was by inverse probability weighting and E-values. Data were analyzed in RStudio. The highest ASDR of 884/10,000 live births was amongst Non-Hispanic Asians and Pacific Islanders in Nevada in 2016–2020. The 2005–2018 median ASDR rose >12-fold in Nevada and New Mexico, >6-fold in New York, and 4.2-fold nationally 1989–2020; it doubled in NY from 2012–2016 to 2016–2020. The average state ASDR rose supra-exponentially (p = 0.0075) and was associated with higher cannabis use states (p = Zero, Cohen’s D = 1.24), apparently driven by cannabis legalization (p = Zero). Estimated exposures to Δ9THC, cannabidiol and cannabigerol were implicated (from p = 2.67 × 10–68). Cannabis-legal states were compared with others (mean ASDR (C.I.) 178.15 (131.68, 224.62) vs. 74.28 (70.60, 77.96), p = Zero; O.R. 1.82 (1.81, 1.84), E-values 3.04 (lower C.I. 3.02), Cohen’s D 1.29 (0.96, 1.62)). Overall, 29/39 (74.4%) E-value estimates were >4; 39/39 (100%) were >1.25. Cannabis, cannabinoids and cannabis legalization are strong candidates for driving the US ASDR supra-exponentially. Estimates of many cannabinoids, including cannabidiol, Δ9THC, and cannabigerol, are implicated. The results are consistent with other large epidemiological studies. The importance of the results is magnified by the increasing legalization and penetration of cannabinoids into the US population. Since therapeutic abortion is not practiced for ASD, it may be used as a bellwether index of heritable transgenerational cannabinoid genotoxicity and epigenotoxicity associated with cannabinoid exposure.
Keywords:
cannabis; cannabinoid; congenitalanomalies; cardiogenesis; genotoxicity; epigenotoxicity; transgenerational inheritance; teratogenesis; multigenerational
(Source: https://www.mdpi.com/2039-4713/16/2/43)
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For years, the conversation about cannabis has centred on mental health, dependency, and the gateway drug debate. Those are serious concerns. But scientific research is now pointing to something far less discussed: the relationship between cannabis exposure and cancer, including acute myeloid leukaemia (AML), one of the most aggressive blood cancers in existence.
The risk does not stop with the person using cannabis. Evidence shows the damage to DNA can be passed on to children who have never used cannabis at all.
Cannabis and AML: What the Data Shows
Multiple large-scale epidemiological studies, drawing on data from both the United States and Europe, have linked cannabis use to a range of cancers including AML, acute lymphoid leukaemia (ALL), breast, thyroid, liver, and pancreatic cancers.
A 2021 study published in Scientific Reports by Reece and Hulse examined US cancer and drug use data from 2003 to 2017. The researchers found that cannabis, THC, cannabigerol, and cannabichromene fulfilled causal criteria for AML, along with thyroid, liver, breast, and pancreatic cancers. The findings held up after controlling for ethnicity, income, and other drug use, with effect sizes ranging from medium to large.
The European data points the same way. A 2023 study published in the Journal of Xenobiotics by Reece, Bennett, and Hulse analysed cancer incidence data from the European Cancer Information System covering 2000 to 2020. Countries with high cannabis use had significantly higher cancer rates. Of 41 cancers examined, 25 were causally linked to cannabis exposure in multivariate models. Compared directly with tobacco and alcohol, cannabis was the stronger correlate of cancer incidence.
When the Damage Is Inherited: Childhood Cancer and the Transgenerational Risk
One of the most serious dimensions of cannabis and AML research involves children. Some cases of AML develop in early childhood, before the age of ten. These children have had no opportunity to use cannabis themselves. Their disease appears to reflect damage inherited from a parent who did.
Research published in 2023 examining sperm DNA methylation in cannabis-dependent individuals found that withdrawal from cannabis triggered 6.5 times more AML-related gene activations than cannabis dependence itself. The hypothesis is that the withdrawal involved in birth, when a newborn is no longer receiving cannabis compounds through the placenta, may activate leukaemogenic gene expression in children born to cannabis-using parents.
This is not a speculative claim. Earlier work from the Children’s Cancer Group in the United States and Canada had already identified a relationship between parental cannabis use and childhood non-lymphoblastic leukaemia. More recent genomic and epigenomic research has provided a mechanism: cannabinoids disrupt DNA methylation patterns in sperm and eggs in ways that carry through to the next generation.
How Cannabinoids Damage DNA
Cannabis genotoxicity, its capacity to damage genetic material, has been documented for more than fifty years. What has changed is our understanding of just how extensive that damage is.
Cannabinoids are toxic to actin and tubulin, the structural proteins cells rely on when they divide. This disrupts the mitotic spindle and can cause chromosomes to separate incorrectly. They also generate reactive oxygen species that damage cell membranes, including those surrounding micronuclei, small packets of fragmented chromosomal material. When those membranes rupture, the result can be chromothripsis, a catastrophic shattering of whole chromosome segments and a known driver of aggressive malignancies.
The genotoxic impact is not limited to THC. Cannabigerol (CBG) and cannabichromene (CBC) have both been implicated in cancer-related chromosomal damage. Even cannabidiol (CBD), widely marketed as safe, has appeared in research as a carcinogenic risk factor for liver and other cancers. The cannabinoid cancer risk appears to run across the entire class, not just the psychoactive compounds.
Dose-response relationships follow exponential and supra-linear curves, meaning risk escalates sharply with increasing exposure rather than rising at a steady rate.
What Legalisation Is Doing to the Data
The Reece and Hulse studies in the US found that jurisdictions that had liberalised cannabis laws had higher cancer rates, rising faster than in non-liberal states, after adjusting for income, ethnicity, and other drug use. Legalisation correlated with worse cancer outcomes, including those associated with cannabis and AML.
Since 1975, the rate of acute lymphoid leukaemia in children under 20 in the US has risen by over 93 per cent. Total paediatric cancer rates rose 42 per cent between 1975 and 2017. Research published in BMC Cancer in 2021 identified cannabis exposure as a major driver of paediatric ALL rates across the United States, with the signal confirmed through spatiotemporal and causal inferential modelling.
Cannabis and AML in Context: A Broader Carcinogenic Picture
AML is not the only blood cancer linked to cannabinoid exposure. Both Hodgkin and non-Hodgkin lymphomas, chronic lymphoid leukaemia, and chronic myeloid leukaemia have appeared in the European datasets. Combined with reproductive cancers of the testis, ovary, prostate, and breast, the pattern strongly implicates damage to germline DNA, the genetic material in sperm and eggs.
Testicular cancer has received particular attention. Meta-analyses have shown that cannabis exposure elevates testicular cancer risk by a factor of approximately 2.6, with development appearing to be significantly accelerated. Researchers estimated an oncogenic rate-incubation index around six times greater than baseline.
The chapter by Reece and Hulse in the 2023 Elsevier volume Cannabis, Cannabinoids, and Endocannabinoids draws on the convergent US and European data and concludes that cannabinoid genotoxicity operates at the scale of hundreds of megabases of the human genome. This is not a targeted mutation. It is broad-spectrum chromosomal disruption.
The Case for Prevention
The research linking cannabis and AML, including acute myeloid and childhood ALL, has moved well beyond early-stage correlation. Multiple independent datasets across different nations, using inverse probability weighting, causal inference models, and spatiotemporal analysis, reach the same conclusions.
Cannabis is a genotoxin. Its carcinogenic risk rivals and in some analyses exceeds that of tobacco. Unlike tobacco, the genetic damage it causes can be inherited. A parent who uses cannabis today may be placing a child not yet born at risk of leukaemia in their first decade of life.
Prevention matters here. Not as a footnote, but as a direct response to what the evidence shows. Every informed choice not to use cannabis is one that may protect more than just the person making it.
(Source: WRD News)
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Alarming new research shows marijuana academic performance links are far more serious than previously thought. Columbia University scientists have uncovered how cannabis damages young people’s school grades, with even occasional use causing significant educational struggles.
The groundbreaking study analysed data from over 160,000 American students. Researchers found that adolescents using marijuana near-daily were almost four times as likely to achieve poor grades compared to non-users.
Marijuana Academic Performance Suffers at Any Usage Level
The findings reveal that cannabis school grades decline even with minimal use. Teenagers consuming marijuana just once or twice monthly reported higher rates of depression, anxiety, and impulsive behaviour than those who abstained entirely.
Dr Ryan Sultán led the research at Columbia University Vagelos College of Physicians and Surgeons. “Previous studies focused on frequent cannabis use amongst teens. Our study found that any amount may put kids at risk of falling behind in school,” he explains.
The research arrives at a critical moment. One in five high school students currently use cannabis. Six percent of final-year students use it daily, a rate that has climbed substantially over the past decade.
How Cannabis School Grades Drop with Regular Use
Near-daily users showed the worst academic outcomes. These students were frequently disengaged from school activities. The negative associations proved even stronger for younger users, raising particular concerns about early adolescent consumption.
“A few joints can snowball into real academic consequences,” Dr Sultán warns. “Teens using it regularly struggle to focus and miss school. They may lose interest in their future plans entirely.”
Brain Development At Stake
Today’s cannabis products contain two to three times more THC than previous generations. This makes them significantly more potent and potentially more harmful. During adolescence, the brain develops critical neural connections that support learning and emotional regulation.
Dr Tim Becker co-authored the study. He serves as assistant professor at Weill Cornell Medicine. “A teenager’s brain is still developing circuits for learning, self-control, and emotional regulation,” he explains. “Using cannabis during these critical periods interferes with those processes. It can derail normal development.”
The study examined students from 2018 to 2022. Over one quarter of respondents reported some cannabis use. Less than 20 percent reported monthly or less frequent use. Much smaller percentages used cannabis weekly or almost every day.
Warning Signs That Cannabis School Grades Are Suffering
Experts recommend frank conversations with teenagers about marijuana early and often. Parents should watch for warning signs including declining grades, mood changes, or loss of interest in hobbies.
“Make sure they understand that natural doesn’t mean safe,” Dr Sultán advises. “It’s not uncommon for a young teen to smoke marijuana only a few times before showing signs of withdrawal. Worsening mood often follows quickly.”
The research provides crucial evidence as cannabis legislation discussions continue. The findings highlight real impacts on young people’s educational futures and emotional wellbeing. Understanding the marijuana academic performance connection has never been more important for educators, parents, and policymakers
(Source: WRD News)
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