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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)

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Published: 22 January 2026

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Unlocking the Biological Impact of Developmental Cannabis and Its Psychiatric Risk

IASIC Speaker Series presents: Dr. Yasmin Hurd, an internationally recognized neuroscientist and leader in translational addiction research. In her talk, “Unlocking the Biological Impact of Developmental Cannabis and Its Psychiatric Risk,” Dr. Hurd will explore cutting-edge evidence on how cannabis exposure during critical developmental periods can alter brain biology and increase vulnerability to psychiatric and substance use disorders later in life. Drawing from decades of preclinical and clinical research, her presentation will provide important insights for researchers, clinicians, and prevention leaders navigating the evolving landscape of cannabis normalization and policy. (I.A.S.I.C)

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Published: 22 January 2026

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The conversation around cannabis has shifted dramatically over the past decade. As legalisation sweeps across nations and the substance becomes increasingly normalised, a troubling pattern has emerged in medical research that demands urgent attention. The link between cannabis and heart attack risk has become undeniable, with young, seemingly healthy adults experiencing cardiac events at rates that have left cardiologists alarmed.

The Six-Fold Risk That Changed Everything

In March 2025, research published in JACC Advances sent shockwaves through the medical community. The study examined over 4.6 million adults under the age of 50, people who should be at their cardiovascular peak. These weren’t individuals with pre-existing heart conditions, high blood pressure, or unhealthy cholesterol levels. They didn’t have diabetes. They didn’t smoke tobacco. By every traditional measure, they should have been safe from heart attacks.

Yet those who used cannabis faced a staggering reality: they were more than six times as likely to suffer a heart attack compared to non-users.

The numbers tell an even grimmer story. Cannabis users in this study also demonstrated a four-fold increased risk of stroke, double the risk of heart failure, and triple the risk of dying from cardiovascular events. These aren’t marginal increases. They represent a fundamental threat to heart health that has gone largely unrecognised by the public.

When Daily Use Becomes Deadly: Cannabis and Heart Attack Risk

A separate study examining 430,000 American adults, published in the Journal of the American Heart Association, revealed the dose-dependent nature of cannabis and heart attack risk. Daily users showed 25% higher odds of heart attack and 42% higher odds of stroke compared to those who abstained entirely; the more frequently someone used cannabis, the higher their cardiovascular risk climbed.

What makes these findings particularly significant is their rigour. Researchers controlled for every confounding factor they could identify: tobacco use, alcohol consumption, body mass index, diabetes, physical activity levels. The cardiovascular risks persisted regardless. Even among people who had never touched a cigarette or vaping device, cannabis use independently increased their chances of heart attack and stroke.

How Cannabis Damages Your Heart

Understanding why cannabis harms the heart requires looking at the body’s endocannabinoid system. This complex network of receptors exists throughout the cardiovascular system, including in the heart muscle itself, blood vessel walls, and the cells that line our arteries.

THC, the primary psychoactive compound in cannabis, activates cannabinoid receptors in ways that trigger a cascade of harmful effects. It promotes oxidative stress—essentially, it causes cells to rust from the inside out. It sparks inflammation in blood vessel walls, the first step in atherosclerosis. It interferes with how the heart contracts, reducing its pumping efficiency.

Cannabis also wreaks havoc on the autonomic nervous system, which regulates heart rate and blood pressure. Within minutes of use, heart rate can spike dramatically while blood pressure swings unpredictably. This combination forces the heart to work harder precisely when blood flow may be compromised—a perfect storm for triggering a cardiac event.

Research has documented that the risk of heart attack peaks within the first hour after cannabis use, suggesting an acute trigger effect similar to other major cardiac stressors.

The Stroke Connection You Need to Know

Whilst heart attacks dominate headlines, the cannabis stroke risk deserves equal attention. The same 2025 research found that younger adults who used cannabis had significantly elevated stroke risk, even without traditional risk factors like high blood pressure or tobacco use.

Cannabis appears to affect stroke risk through multiple mechanisms. It can cause blood vessels in the brain to constrict abnormally. It promotes blood clotting. It triggers inflammatory responses in vessel walls. The combination creates dangerous conditions for both ischaemic strokes (caused by blocked blood flow) and potentially haemorrhagic strokes (caused by bleeding).

For young people who believe strokes only affect the elderly, this represents a profound wake-up call. The research demonstrates that cannabis use fundamentally alters cerebrovascular function in ways that put users at immediate risk.

200 Million People Can’t Be Wrong

A meta-analysis examining 24 studies involving approximately 200 million people confirmed what individual studies suggested. Published in the journal Heart, this systematic review found that cannabis users faced a 29% higher risk of acute coronary syndrome, a 20% higher risk of stroke, and. Most alarming, a doubled risk of dying from cardiovascular disease.

These aren’t isolated findings from a single laboratory or region. The research spans multiple countries, diverse populations, and various study designs. Ten studies were conducted in the United States, with additional research from Canada and India. Seven found significant positive associations between cannabis and heart attacks, whilst the pooled data conclusively demonstrated a 50% increased risk.

The consistency across this research is striking. When hundreds of millions of data points from independent studies all point in the same direction, it becomes impossible to dismiss the connection as coincidence.

Vaping and Edibles Won’t Save You

Some advocates have suggested that smoking cannabis specifically poses risks, but that other consumption methods might be safer. The evidence doesn’t support this comforting narrative.

Studies examining cannabis use found elevated cardiovascular risks whether people smoked, vaped, or consumed edibles. Whilst smoking introduces additional particulate matter that damages blood vessels, the fundamental problem lies with THC itself and how it interacts with the cardiovascular system.

Cannabis smoke does contain many of the same toxic compounds as tobacco smoke—particulate matter, oxidant gases, carbon monoxide. These substances activate platelets, promote oxidised cholesterol formation, and trigger inflammatory responses. But even when researchers isolated cannabis users who had never smoked anything, the cardiovascular risks remained significantly elevated.

K2 and Spice: Even More Dangerous

If traditional cannabis poses substantial cardiovascular risks, synthetic cannabinoids represent an exponentially greater danger. Products marketed as K2, Spice, and similar brands contain compounds that are full agonists of cannabinoid receptors—meaning they activate these receptors completely, unlike THC which only partially activates them.

These synthetic substances can be hundreds of times more potent than natural cannabis. They’ve been linked to severe cardiac emergencies including sudden cardiac arrest from dangerous heart rhythm abnormalities, acute heart attacks in otherwise healthy young people, and catastrophic strokes.

Critically, standard drug tests don’t detect synthetic cannabinoids, making it difficult for medical professionals to identify exposure when users present with cardiac emergencies.

Why Doctors Are Sounding the Alarm

As cannabis legalisation expands globally and social attitudes shift towards acceptance, consumption rates have climbed, particularly among younger demographics. The 2025 research reveals that this trend coincides with cardiovascular risks that public health messaging has largely failed to communicate. Understanding cannabis and heart attack risk has become critical for anyone making informed decisions about their health.

The researchers behind these studies have called for cannabis to be treated as a serious cardiovascular risk factor, on par with tobacco smoking, hypertension, and high cholesterol. Dr Ibrahim Kamel, lead author of the landmark 2025 study, stated: “At a policy level, a fair warning should be made so that people who are consuming cannabis know that there are risks.”

Yet public perception lags dangerously behind the science. Legalisation and medical cannabis programmes have inadvertently fostered the belief that cannabis is benign. The cardiovascular research tells a different story entirely.

Is Any Amount Safe? Cannabis and Heart Attack Risk

The dose-dependent relationship observed in multiple studies, where more frequent use correlates with higher cardiovascular risk, suggests there’s no threshold where cannabis and heart attack risk disappears entirely. Daily users face the highest risks, but even occasional use shows elevated cardiovascular danger compared to abstinence.

This presents a clear message: from a cardiovascular standpoint, any cannabis use carries risk. For young people who believe they’re invulnerable, for individuals with undiagnosed heart conditions, for anyone with a family history of cardiovascular disease, that risk could prove fatal.

Where You Stand on the Risk Scale

Cardiovascular disease remains the leading cause of death globally. The addition of cannabis as a significant, modifiable risk factor changes the prevention landscape fundamentally.

Traditional risk factors. Smoking, obesity, sedentary lifestyle, poor diet, hypertension: remain critical. But the emerging evidence demonstrates that cannabis use independently elevates risk, potentially turning someone who would otherwise be safe into someone vulnerable to life-threatening cardiac events.

The research indicates that asking about cannabis use should become standard practice in cardiovascular risk assessment, alongside questions about tobacco, exercise, and family history. For individuals making informed decisions about their health, this information is essential.

Major Medical Organisations Agree

The scientific consensus emerging from this research is unambiguous. Major cardiovascular organisations including the American Heart Association and the American College of Cardiology have published statements acknowledging the cardiovascular risks of cannabis use.

Editorials accompanying the research have called for cannabis to be actively discouraged from a public health standpoint, with particular protection for vulnerable populations. The comparison to tobacco is deliberate. Both substances carry serious cardiovascular risks that public policy should address.

Researchers emphasise the need for continued investigation into mechanisms, dose-response relationships, and population-specific vulnerabilities. But the foundation of evidence is already substantial enough to warrant serious concern and immediate public health action.

The Bottom Line on Cannabis and Your Heart

This body of research represents a turning point in our understanding of cannabis and cardiovascular health. The evidence is no longer preliminary, isolated, or ambiguous. Multiple large-scale studies involving millions of participants have demonstrated clear, consistent, and alarming associations between cannabis use and serious heart disease.

For individuals, the message is straightforward: cannabis use significantly elevates the risk of heart attack, stroke, heart failure, and cardiovascular death. This risk exists independently of other factors, affects young people who should be at low cardiovascular risk, and increases with frequency of use.

The choice to use cannabis is ultimately personal, but it should be an informed choice based on accurate understanding of genuine risks. The research published in 2024 and 2025 provides that information with unprecedented clarity.

Hearts are remarkable organs, resilient and powerful. But they’re not invincible, and the evidence demonstrates that cannabis use represents a serious, preventable threat to cardiovascular health. In an era where heart disease remains our greatest health challenge, adding unnecessary risk factors makes little sense.

The conversation around cannabis has focused heavily on legalisation, medical applications, and social justice. It’s past time the discussion included the cardiovascular consequences that research has now conclusively documented.

Your heart deserves better than wishful thinking and outdated assumptions. It deserves decisions based on the best available science. And that science speaks clearly about the dangers cannabis poses to cardiovascular health.

References

1. Kamel I, Mahmoud AK, Twayana AR, et al. Myocardial Infarction and Cardiovascular Risks Associated with Cannabis Use: A Multicenter Retrospective Study. JACC Adv. 2025. https://www.acc.org/About-ACC/Press-Releases/2025/03/17/15/35/Cannabis-Users-Face-Substantially-Higher-Risk
2. Jeffers AM, Glantz S, Byers AL, Keyhani S. Association of Cannabis Use With Cardiovascular Outcomes Among US Adults. J Am Heart Assoc. 2024;13(5):e030178. https://www.ahajournals.org/doi/10.1161/JAHA.123.030178
3. Cardiovascular risk associated with the use of cannabis and cannabinoids: a systematic review and meta-analysis. Heart. 2024. https://bmjgroup.com/cannabis-use-linked-to-doubling-in-risk-of-cardiovascular-disease-death/
4. Chandy M, Jimenez-Tellez N, Wu JC. The relationship between cannabis and cardiovascular disease: clearing the haze. Nat Rev Cardiol. 2025;22:467-481. https://www.nature.com/articles/s41569-025-01121-6