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Published: 10 March 2026

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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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Published: 15 February 2026

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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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Published: 05 February 2026

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‘A large phase 3 trial in Nature Medicine has delivered a ‘stronger’ clinical signal that a proprietary cannabis extract, VER-01, can modestly reduce chronic low back pain – but the effect is small, side effects are common, and broader evidence from other pain conditions remains weak and inconsistent. Experts say the findings should temper rather than fuel enthusiasm, especially for general cannabis use or over-the-counter products.

Trial highlights: modest benefit over placebo (a very close second)

The multicentre randomized controlled trial enrolled 820 adults with chronic low back pain and compared VER-01, a standardized full‑spectrum Cannabis sativa extract containing THC, CBD and other cannabinoids, with placebo over 12–15 weeks, followed by extension phases.¹

Key efficacy findings include:

• Average pain reduction of 1.9 points on an 11‑point numeric rating scale (NRS) with VER‑01 vs 1.3–1.4 points with placebo, producing a mean between‑group difference of about −0.6 NRS points (95% CI roughly −0.9 to −0.3).²
• About 42% of VER‑01 patients achieved at least 30% pain reduction vs 31% on placebo, giving a number needed to treat (NNT) of 6.8 for this threshold.³  
• Secondary outcomes showed statistically significant improvements in sleep quality, physical function and patient global impression of change, with reduced use of rescue analgesics.⁴

Clinically, that means most participants in both arms felt somewhat better, but only a minority derived clearly meaningful extra benefit from VER‑01 beyond placebo, and the average advantage was modest.⁵

Safety profile: frequent adverse effects, limited durability

VER‑01’s safety signal is not benign. Adverse events (AEs) were substantially more common in the active arm:

• Any AE occurred in 83.3% of VER‑01 recipients vs 67.3% on placebo, mostly dizziness, fatigue, somnolence, nausea and related nervous‑system symptoms.⁶
• Treatment discontinuation due to AEs was around 17% with VER‑01 compared with 3.5% on placebo.⁷
• In the randomized withdrawal phase, VER‑01 did not significantly prolong time to treatment failure compared with placebo (HR 0.75; p=0.288), suggesting limited durability or strong contextual/placebo contributions. ⁸

Importantly, the trial reports no clear signals of abuse, dependence or withdrawal in the controlled period or the six‑month open‑label extension, but the follow‑up is still relatively short for judging long‑term neurocognitive or psychiatric risks. The absence of formal blinding checks and dedicated cognitive testing leaves some uncertainty about expectation effects and subtle harms.⁹

What the broader evidence shows: small gains, real harms

The VER‑01 findings sit within a larger, more sobering evidence base on cannabis‑based medicines for chronic pain. A major Cochrane review of 16 randomized trials (n=1,750) in chronic neuropathic pain – using oral THC/CBD sprays, synthetic THC (nabilone), dronabinol, and smoked herbal cannabis – found only small benefits and clear safety concerns.

Across pooled neuropathic pain studies, the review reported:

• 50% pain relief: 21% with cannabis‑based medicines vs 17% with placebo (risk difference 0.05; NNT ≈ 20; low‑quality evidence).
• 30% pain relief: 39% vs 33% (risk difference 0.09; NNT ≈ 11; moderate‑quality evidence).
• Withdrawals due to adverse events: 10% vs 5% (NNH ≈ 25; moderate‑quality evidence).
• Any nervous‑system AE (e.g. dizziness, somnolence): 61% vs 29% (risk difference 0.38; NNH ≈ 3).
• Psychiatric AEs (e.g. confusion, mood or perceptual changes): 17% vs 5% (risk difference 0.10; NNH ≈ 10).

The authors concluded that “the potential benefits of cannabis‑based medicine… in chronic neuropathic pain might be outweighed by their potential harms” and that there is no high‑quality evidence supporting any cannabis‑based product for chronic neuropathic pain. Evidence for smoked or herbal cannabis was rated very low quality and showed no clear advantage over placebo.

Although neuropathic pain differs from mechanical low back pain, both are chronic pain states in which placebo responses are high and NNTs for cannabis‑based products tend to cluster in the 6–20 range, with frequent nervous‑system and psychiatric adverse events. This broader context undercuts simple narratives that “cannabis works for chronic pain” and suggests any benefit is typically modest and tightly bound to specific formulations and trial conditions.¹⁰ 

Experts urge caution: specific product, specific setting

Though some investigators of this trial had a clear conflict of interest, which the literature hasn’t made clear, some specialists commenting on the VER‑01 trial have welcomed it as a methodologically stronger study than most past cannabis pain trials, (which quality and depth have all been very sub-standard) but stress several caveats:

• The results are specific to VER‑01 – a standardized, pharmaceutical‑grade extract – and cannot be generalized to smoked cannabis, edibles, or unregulated oils.¹¹
• The effect size is small; in practice, it equates to about a 30% average pain reduction on VER‑01 vs 20% on placebo over 12 weeks.^12​
• Given Cochrane’s finding that cannabis‑based medicines for neuropathic pain offer only minor additional benefit over placebo with substantial nervous‑system and psychiatric AEs, routine first‑line use in back pain would be hard to justify.

Guidelines cited by the Cochrane review generally position cannabis‑based medicines, if considered at all, as third‑ or fourth‑line options after established treatments such as NSAIDs, antidepressants, anticonvulsants, and non‑pharmacologic therapies have been tried and found inadequate. Some expert groups even give a weak recommendation against routine use in neuropathic pain because of low‑quality benefits and safety concerns.

What this means for patients, clinicians and policy

Taken together, the VER‑01 trial and the Cochrane synthesis point to a cautious, tightly targeted role for cannabis‑based medicines in chronic pain:

• Not a miracle drug: VER‑01 offers statistically significant but clinically modest improvements in chronic low back pain; placebo comes a close second on most endpoints.¹³
• Meaningful benefit for a minority: NNTs around 6–11 for 30% pain relief – in both VER‑01 and the neuropathic pain literature – imply that many patients will not gain substantial extra benefit over optimized standard care.^14​
• Real risk of side effects: Dizziness, somnolence, cognitive and psychiatric symptoms are common, with NNHs as low as 3 for nervous‑system events in neuropathic pain trials, and discontinuation rates notably higher than placebo in both VER‑01 and Cochrane data.^15  ​
• Formulation matters: Evidence supports specific, trial‑tested preparations (like VER‑01 or THC/CBD oromucosal sprays), not generic plant material or over‑the‑counter products.¹⁶  ​
• Research, not routine: Longer‑term safety, comparative effectiveness vs opioids, NSAIDs and guideline‑recommended non‑drug therapies, and performance in more heterogeneous real‑world populations all remain open questions.¹⁷ ​

For now, chronic low back pain patients and clinicians may reasonably view VER‑01 as a potential non‑opioid option for carefully selected individuals who have not responded to established treatments and who accept a high likelihood of transient but bothersome side effects. Yet in light of the broader evidence base, these new data are better seen as an incremental advance than as proof that cannabis, in general, reliably and safely relieves chronic back pain.^18 ​

For complete research – Major Sources

• Cannabis‐based medicines for chronic neuropathic pain in adults - Mücke, M - 2018 | Cochrane Library
• Full-spectrum extract from Cannabis sativa DKJ127 for chronic low back pain: a phase 3 randomized placebo-controlled trial
• No clear evidence that cannabis-based medicines relieve chronic nerve pain | Cochrane

Dalgarno Institute

 

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Published: 27 January 2026

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The argument surfaces repeatedly in public debates: if society tolerates alcohol, why not cannabis? It’s a question that sounds reasonable until you examine what science actually tells us about marijuana vs alcohol.

According to Harvard Medical School professor Dr Bertha K. Madras, a psychobiologist with decades of research into addiction and neurobiology, this comparison rests on shaky ground. Whilst alcohol undoubtedly causes significant harm, treating marijuana and alcohol as interchangeable risks ignores crucial differences that matter for public health.

About 60% of US adults use alcohol sometime each year, whilst only 15% use cannabis. Yet the consequences tell a surprising story.

Medical Impacts: Comparison Of Marijuana And Alcohol

Take one of the most common comparisons: both substances can make people sick. Advocates often point to alcohol-induced vomiting as equivalent to what cannabis users experience. Dr Madras draws a sharp distinction.

Alcohol-related vomiting typically occurs as an acute toxic response. Your body reacting to excessive intake in a single episode. Once you stop drinking and recover, the symptoms resolve. Unpleasant, certainly, but temporary.

Cannabis hyperemesis syndrome tells a different story entirely. This chronic disorder develops after long-term heavy marijuana use and causes cyclical episodes of severe, relentless vomiting that can occur dozens of times daily. Patients endure significant abdominal pain, and standard anti-nausea medications often prove useless. Many resort to compulsive hot showers for temporary relief.

The condition leads to repeated emergency department visits, severe dehydration, and electrolyte disturbances. The only known effective treatment? Complete abstinence from cannabis. This isn’t an episodic response to overindulgence. It’s a chronic medical syndrome triggered by the drug itself.

Psychiatric Risks: Cannabis vs Alcohol

Another frequent claim suggests that alcohol-induced psychosis and cannabis-induced psychosis carry similar long-term risks. The research contradicts this assumption when examining marijuana vs alcohol effects on mental health.

Dr Madras points to longitudinal studies showing that people who experience psychosis following marijuana use face substantially higher rates of conversion to schizophrenia compared to those whose psychosis stems from alcohol. This isn’t a minor statistical blip. Individuals affected by cannabis-induced psychosis are far more likely to develop chronic psychotic disorders.

The observation isn’t new. As far back as the 19th century, the Indian Hemp Drugs Commission documented stronger associations between cannabis use and psychotic illness than with alcohol. Modern research has repeatedly confirmed this relationship, particularly amongst adolescents and young adults whose brains haven’t finished developing.

Acknowledging this difference doesn’t excuse alcohol’s psychiatric harms. It simply challenges the notion that marijuana and alcohol pose the same mental health risks.

Public Health Consequences Beyond Individual Choice

Some argue that even if cannabis carries unique harms, adults should remain free to make their own decisions. Dr Madras cautions that this framing misses the broader picture when considering marijuana vs alcohol policy.

“Why should marijuana be treated the same as alcohol, by adding it to our already long list of drug-related public health crises?” she asks.

The evidence suggests cannabis use is strongly associated with subsequent opioid misuse. Research links it to greater adverse effects on educational attainment compared to alcohol. High-potency cannabis products appear to carry higher addictive potential than alcoholic drinks. These outcomes don’t just affect individual users. They ripple through families, schools, healthcare systems, and entire communities.

The effects span generations too. When adults use marijuana, particularly parents, their children and young adults aged 12 to 30 become substantially more likely to use it themselves. The idea that adult use exists in isolation from youth exposure doesn’t hold up under scrutiny.

How Marijuana And Alcohol Differ Chemically

The cannabis products available today bear little resemblance to those from previous decades. Potency has increased dramatically, driven by what some describe as an addiction for profit industry. This matters because of how the substances work in the body.

Alcohol is water soluble. The effects of a standard drink last roughly an hour as your body processes and eliminates it. Cannabis, being fat soluble, behaves differently. The impacts of marijuana ingestion can persist for multiple hours, even days, as the compounds remain stored in body fat and gradually release.

Both drugs carry dangers, but the pharmacological differences mean the risks don’t map neatly onto each other.

The Road Safety Reality With Cannabis And Alcohol

Perhaps nowhere is the marijuana vs alcohol comparison more troubling than in traffic safety data. Despite cannabis use rates sitting at roughly 15% of adults compared to 60% for alcohol, marijuana impaired driving deaths and injuries are now rivalling alcohol related crash statistics.

Usage patterns tell part of the story. About one in ten alcohol users drink daily. Among regular cannabis users, that figure jumps to one in two using every day. The implications for impaired driving become clearer when you consider both the frequency of use and how long the effects persist.

What The Evidence Tells Us About Marijuana Vs Alcohol

Alcohol remains a serious public health problem deserving continued attention and intervention. Recognising cannabis carries distinct risks doesn’t minimise alcohol’s harms or suggest we should be complacent about alcohol policy.

It simply rejects the logic that one harmful substance justifies adding another to the mix.

As Dr Madras concludes, marijuana should be treated differently from alcohol “because it is different, in its clinical syndromes, psychiatric risks, developmental consequences, and intergenerational effects.”

Effective public health policy depends on recognising those differences rather than papering over them with false equivalence. The question isn’t whether society already tolerates one harmful drug. It’s whether evidence supports treating two different substances as though they pose the same risks.

The science suggests they don’t.

(Source: WRD News)