For those looking to reduce their chances of developing lung disease, say experts at UC San Francisco, then it may be smart to avoid inhaling cannabis.
A new study in the Journal of General Internal Medicine found that inhaling marijuana every day is associated with a 44% increased chance of developing asthma. It also increases the odds of developing a common set of lung diseases known as chronic obstructive pulmonary disease (COPD) by 27%.
The risk of COPD, which includes emphysema and chronic bronchitis, may be understated. The disease takes decades to develop, and the researchers did not have detailed information on how long people in the study had been using cannabis.
Researchers defined “inhaling” as smoking, vaping, and so-called “dabbing,” which involves breathing in the vapors of concentrated marijuana. The study found an association between elevated risks to a person’s lungs and doing any of those things with cannabis even for those who had never smoked cigarettes.
For those who never smoked cigarettes, inhaling marijuana every day was linked to a 51% increased likelihood of developing asthma. The association with COPD was also elevated, but it was not statistically significant.
The study is the largest yet to examine the association between inhaling cannabis and risks to respiratory health among people who have not smoked cigarettes. Of the 380 000 adult participants, nearly 222 000 had never smoked tobacco. The data comes from the Behavioral Risk Factor Surveillance System, a national survey by the Centers for Disease Control and Prevention (CDC).
Experts say the broad legalization of marijuana across much of the country and the perception that it is healthier than tobacco has led people to minimize the risks.
“The message about smoking tobacco being bad for you has gotten out there, but for cannabis, it’s much less clear,” said Alison Rustagi, MD, PhD, assistant professor at UCSF and first author of the paper.
“If people are looking to reduce their likelihood of developing a chronic lung disease, they should not start using cannabis,” she said. “And if they already smoke cannabis, they should do it less often.”
With females aged 25-34 showing a 255 percent surge in alcohol-related deaths during this time period
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In an analysis by race, sex, age, and geography, alcohol-induced death rates in 2024 are nearly double those in 1999, with a sharp increase at the onset of the COVID-19 pandemic. Although rates are higher for men, the largest increase in alcohol-induced deaths over the full 25-year period occurred in females aged 25-34, according to a study published on September 17 by Dr Tony Wong and colleagues at UCLA in the open-access journal PLOS Global Public Health.
Alcohol-induced deaths have been increasing over the past two decades. Particularly concerning are increases between 2019 and 2021, when the population was under significant stress from isolation due to the COVID-19 pandemic, and people with alcohol-use disorders were less able to access treatment. Quantifying mortality trends and determining whether alcohol-induced deaths have returned to pre-pandemic levels is essential for understanding long-term temporal patterns and dynamics. To examine these trends, the authors of this study analysed data from the Centers for Disease Control and Prevention’s National Vital Statistics System, focusing on 14 specific alcohol-induced causes of death.
Wong et al. found that rates of alcohol-induced deaths in the United States nearly doubled between 1999 and 2024, reaching their highest level in 2021. Most deaths are due to alcoholic liver disease and, to a lesser degree, alcohol-related mental and behavioural disorders. The largest overall increase in alcohol-induced mortality across all race, sex, age groups occurred in 2021 when fatalities peaked at 54,258 deaths overall. By 2024, fatalities had declined, but the average alcohol-induced mortality rate across U.S. counties remained approximately 25% higher than in 2019.
American Indian/Alaska Native populations (AIAN) remain the most affected, with male AIAN rates of alcohol-induced mortality three times higher than that of white males, and female AIAN mortality rates four times higher than that of white females, over the entire period of investigation.
The largest increase by demographic was among females aged 25-34, which rose from 0.9 deaths per 100 000 in 1999 to 3.2 per 100 000 in 2024 — a 255 percent increase. The second largest increase was in males aged 25-34, from 2.3 fatalities per 100 000 in 1999 to 6.5 in 2024 — a 188 percent increase. As deaths from chronic diseases related to alcohol use, such as certain cancers or cardiovascular events, were not included in this study, the overall fatality counts may be underestimated. These findings underscore the critical need for targeted policies to reduce excessive alcohol consumption and improve access to treatment for those who need it most.
Senior author Maria R D’Orsogna adds: “The rapid rise of alcohol-induced deaths among women is particularly concerning. Although men still die at higher rates, the gender gap appears to be closing. Notably, for the population aged 25-34, the male-to-female mortality ratio has decreased from three-to-one in 1999 to two-to-one in 2024.”
The authors conclude: “The rise in alcohol-induced mortality is widespread and affects the entire country, with particularly large surges arising during the COVID-19 pandemic. In the early months of the pandemic, alcohol-induced deaths among AIAN males increased by as much as 40% in a single month and remained unusually high for nearly four years. Similar trends were observed among AIAN and Black females, whose alcohol-induced death rates rose by over 30% in one month.”
GLP-1 receptor agonists are also promising for the treatment of alcohol use disorder and alcohol-associated liver disease, as growing evidence suggests they reduce the motivation to drink alcohol. Now, surprising new findings reveal that the medications may have direct protective effects on the liver as well.
In a new study, published in npj Metabolism Health and Disease, Yale School of Medicine (YSM) researchers found that in mice, GLP-1RAs reduced an enzyme that metabolises alcohol. That, in turn, decreased the production of toxic alcohol metabolites.
“This is the first time that GLP-1 receptor agonists have been shown to regulate alcohol metabolism in the liver,” says principal investigator Wajahat Mehal, MD, professor of medicine (digestive diseases) at YSM. “If you’re taking semaglutide, then your body will likely handle alcohol differently.”
However, because these drugs slowed the metabolism of alcohol, the mice also had higher blood alcohol levels, the researchers found.
“GLP-1 receptor agonists seem to have very similar effects in mice and humans,” says Mehal. “If these results are also reproduced in humans, people using GLP-1 receptor agonists might be drinking an amount of alcohol that does not normally put them above the legal blood alcohol level, but because they are taking this drug, it does.”
Further studies in humans are needed to understand these impacts of GLP-1 receptor agonists more fully, he stresses.
In the study, researchers gave mice either a GLP-1 receptor agonist or a placebo. They observed that mice receiving the medication had decreased levels of a liver enzyme known as Cyp2e1, which breaks down alcohol into a toxic metabolite called acetaldehyde.
“This is significant because alcohol itself is actually not the most toxic molecule to the liver,” explains Mehal. Rather, acetaldehyde is one of the major drivers of alcohol-related harm to the liver. “These drugs are resulting in less acetaldehyde.”
The findings suggest that not only might GLP-1 receptor agonists help the liver by acting on the brain to reduce alcohol consumption, but also through slowing metabolism of alcohol in the liver, and in turn reducing the levels of toxic metabolites.
Ongoing clinical trials are currently testing the benefits of semaglutide for people living with alcohol-induced liver disease. The study suggests that GLP-1 receptor agonists may offer greater benefits to the liver than previously thought, and that the drug may still help patients who are not abstaining from alcohol.
“Even if some individuals don’t reduce their alcohol intake while they’re on a GLP-1 receptor agonist, they will probably still have hepatic protection, because fewer toxic metabolites will be produced in the liver,” Mehal says.
In another experiment, the researchers measured blood alcohol concentrations of mice 30 minutes after giving them alcohol. They found that mice who had received a GLP-1 receptor agonist had higher blood alcohol concentrations compared to controls, and that these levels took longer to drop.
More research is needed to better understand the consequences of elevated blood alcohol levels on the rest of the body, Mehal says.
“If the liver is not metabolizing alcohol as quickly, the alcohol load could be shifted to other organs,” he poses. “Then, not only might people have a high blood alcohol level, but may also experience more cognitive effects like discoordination.”
The number of people taking these drugs is rapidly increasing—as many as one in eight adults in the U.S. have used or are currently using a GLP-1 receptor agonist. Meanwhile, about half of U.S. adults drink alcohol and 6% report drinking heavily.
As the use of these medications for a range of conditions continues to rise, it is increasingly important to study the interactions between these medications and alcohol, Mehal says.
“There already are large numbers of people who are taking GLP-1 receptor agonists and are drinking either social amounts or excess amounts of alcohol,” says Mehal. “We need to know the effects of these drugs in that setting.
What compels someone to keep engaging in alcohol use, even if it damages their health, relationships and wellbeing? A new study from Scripps Research offers an important clue: a small midline brain region plays a key role in how animals learn to continue drinking to avoid the stress and misery of withdrawal.
In a new study, published in Biological Psychiatry: Global Open Science on August 5, 2025, the Scripps Research team zeroed in on a set of brain cells in the paraventricular nucleus of the thalamus (PVT) in rats. They found that this region becomes more active, driving strong relapse behaviour, when rats learn to associate environmental stimuli with the easing of withdrawal symptoms by alcohol. By illuminating this brain pathway, the research sheds light on one of the most stubborn features of addiction – drinking not for pleasure, but to escape pain – and could eventually lead to new treatments for substance use disorders (SUDs) as well as other maladaptive behaviours including anxiety.
“What makes addiction so hard to break is that people aren’t simply chasing a high,” says Friedbert Weiss, professor of neuroscience at Scripps Research and senior author of the study. “They’re also trying to get rid of powerful negative states, like the stress and anxiety of withdrawal. This work shows us which brain systems are responsible for locking in that kind of learning, and why it can make relapse so persistent.”
“This brain region just lit up in every rat that had gone through withdrawal-related learning,” says co-senior author Hermina Nedelescu of Scripps Research. “It shows us which circuits are recruited when the brain links alcohol with relief from stress – and that could be a game-changer in how we think about relapse.”
From behaviour to brain maps
An estimated 14.5 million people in the United States have alcohol use disorder, which encompasses a range of unhealthy drinking behaviours. Like other drug addictions, alcohol addiction is characterised by cycles of withdrawal, abstinence and relapse.
In 2022, Weiss and Nedelescu used rats to study the types of learning that happen in the brain throughout this cycle. When rats initially begin drinking, they learn to associate pleasure with alcohol and seek more. However, that conditioning becomes far stronger during multiple cycles of withdrawal and relapse. After learning that alcohol eased the unpleasant feelings of withdrawal – negative reinforcement, or a relief of ‘negative hedonic state’ – the animals sought out more alcohol and would remain persistent even when uncomfortable.
“When rats learn to associate environmental stimuli or contexts with the experience of relief, they end up with an incredibly powerful urge to seek alcohol in the presence of that stimuli –even if conditions are introduced that require great effort to engage in alcohol seeking,” says Weiss. “That is, these rats seek alcohol even if that behavior is punished.”
In the new work, the team wanted to pin down exactly what networks of cells in the brain were responsible for learning to associate environmental cues with the relief of this negative hedonic state.
The researchers used advanced imaging tools to scan entire rat brains, cell by cell, and pinpoint areas that became more active in response to alcohol-related cues. They compared four groups of rats: those that had gone through withdrawal and learned that alcohol relieves a negative hedonic state, and three different control groups that had not.
While several brain areas showed increased activity in the withdrawal-learned rats, one stood out: the PVT, which is known for its role in stress and anxiety.
“In retrospect, this makes a lot of sense,” says Nedelescu. “The unpleasant effects of alcohol withdrawal are strongly associated with stress, and alcohol is providing relief from the agony of that stressful state.”
The researchers hypothesise that this negative hedonic state, and the activation of the PVT in the brain as a response, is critical for how the brain learns and perpetuates addiction.
A better understanding of addiction
The implications of the new study extend well beyond alcohol, the researchers say. Environmental stimuli conditioned to negative reinforcement – the drive to act in order to escape pain or stress – is a universal feature of the brain, and can drive human behaviour beyond substance use disorders such as anxiety disorders, fear-conditioning and traumatic avoidance learning.
“This work has potential applications not only for alcohol addiction, but also other disorders where people get trapped in harmful cycles,” says Nedelescu.
Future research will zoom in even further. Nedelescu and colleagues at Scripps Research want to expand the study to females and to study neurochemicals released in the PVT when subjects encounter environments associated with the experience of this relief from a negative hedonic state. If they can pinpoint molecules that are involved, it could open new avenues for drug development by targeting those molecules.
For now, the new study underscores a key shift in how basic scientists think about addiction.
“As psychologists, we’ve long known that addiction isn’t just about chasing pleasure – it’s about escaping those negative hedonic states,” says Weiss. “This study shows us where in the brain that learning takes root, which is a step forward.”
Excessive alcohol consumption can disrupt the liver’s unique regenerative abilities by trapping cells in limbo between their functional and regenerative states, even after a patient stops drinking, as described in a new study from researchers at University of Illinois Urbana-Champaign and collaborators.
This in-between state is a result of inflammation disrupting how RNA is spliced during the protein-making process, the researchers found, providing scientists with new treatment pathways to explore for the deadly disease. The researchers published their findings in the journal Nature Communications.
The liver has a remarkable ability to regenerate itself after damage or partial removal. However, it loses that ability in patients with alcohol-associated liver disease – the leading cause of liver-related mortality worldwide, resulting in roughly 3 million deaths annually.
“We knew that the liver stops functioning and stops regenerating in patients with alcohol-related hepatitis and cirrhosis, even when a patient has discontinued consuming alcohol, but we didn’t know why,” said U. of I. biochemistry professor Auinash Kalsotra, who co-led the study with Duke University School of Medicine professor Anna Mae Diehl. “The only real life-saving treatment option once a patient reaches the liver failure stage in those diseases is transplantation. But if we understood why these livers were failing, maybe we could intervene.”
Both the Kalsotra and Diehl labs havestudied the molecular and cellular underpinnings of liver regeneration. Over the last five years, they found that in order to regenerate, liver cells reprogram their gene expression to revert to fetal-like progenitor cells, multiply and then reverse the process back to become mature functioning cells again. Armed with this knowledge, the group turned to the question of how those mechanisms were disrupted in alcohol-associated liver disease.
The researchers compared samples of healthy livers and samples of livers with alcohol-associated hepatitis or cirrhosis obtained from Johns Hopkins University Hospital through an initiative supported by the National Institute for Alcohol Abuse and Alcoholism, part of the National Institutes of Health.
The first thing the researchers noticed in diseased livers was that, although damaged cells had begun the process of reverting to the regenerative state, they did not complete the process and instead remained in transitional limbo.
“They are neither functional adult cells nor proliferative progenitor cells. Since they are not functioning, more pressure builds on the remaining cells. So they try to regenerate, and they’re all ending up in this unproductive quasi-progenitor state, and that’s what is causing liver failure,” said U. of I. graduate students Ullas Chembazhi and Sushant Bangru, the co-first authors of the study.
To figure out why the cells were getting stuck in this state, the team investigated which proteins were being made by the liver cells and, in turn, the RNA molecules carrying the instructions for those proteins from the DNA to the cell’s protein-building machinery.
While most studies focus only on the total amounts of RNA or protein in a cell, Kalsotra’s team used deep RNA sequencing technology and computational analyses to zoom in on the splicing of RNA fragments, a key step in stitching together different parts of genetic instructions to make proteins.
“In comparing the samples, we saw RNA was getting mis-spliced broadly in alcohol-related liver disease, across thousands of genes, and it was affecting major functions of proteins,” said Kalsotra.
The researchers found a possible driver of the RNA mis-splicing: Alcohol-damaged liver cells had a deficiency of the protein ESRP2, which binds to RNA to splice it properly.
“Proteins function at a very specific place in the cell, and that is directed by sequences within the protein that take the protein to that particular spot. We found that, in many cases, the sequence that dictates where the protein localizes within a cell was mis-spliced. That’s why it was important that we did the multiple analyses we did,” said Kalsotra. “There was the same amount of RNA and protein, but the protein was not at the right place to function. Due to mis-splicing, key proteins that are required for productive liver regeneration were getting stuck in the cytoplasm, when they needed to be in the nucleus.”
To verify that ESRP2 deficiency was a likely culprit, the researchers studied mice without the gene that produces ESRP2. They displayed similar liver damage and regeneration failure to that seen in patients with advanced alcohol-related hepatitis.
But why was ESRP2 missing from liver cells from patients with alcohol-related hepatitis? Upon investigation, the researchers found that liver support cells and immune cells, drawn to the liver tissue damaged by alcohol processing, released high amounts of inflammatory and growth factors. Those factors suppress ESRP2 production and activity.
To verify this finding, the researchers treated liver cell cultures with a molecule that inhibits the receptor for one of the inflammation-promoting factors. ESRP2 levels recovered and splicing activity was corrected, pointing to the pathway as a possible treatment target.
“I’m hopeful these findings will become a launching pad for future clinical studies. We can use these mis-spliced RNAs as diagnostic markers or develop treatments that can curb the inflammation. And if we can correct the splicing defects, then maybe we can improve recovery and restore damaged livers,” Kalsotra said.
New research from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, in partnership with the University of Bath, has found that the reasons why a person chooses to use cannabis can increase their risk of developing paranoia.
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The use and potency of cannabis is increasing worldwide, and dependence and cannabis-induced psychosis are also greatly increasing as a result, especially in North America. Two new research papers, both using data from Cannabis & Me – the largest survey of its kind – have identified key risk factors associated with the more severe forms of paranoia in cannabis users.
The first study, published in BMJ Mental Health, explored the relationship between why people first started using cannabis, and how this affected their subsequent use.
3389 former and current cannabis users aged 18 and over responded to a survey examining their reasons for first and continued use, their weekly consumption of cannabis in THC units, and their mental health.
Researchers established several key findings. Respondents who first started using cannabis to self-medicate an illness, including physical pain, anxiety, depression, or because they were experiencing minor psychotic symptoms, all demonstrated higher paranoia scores.
This was in contrast to those respondents who tried cannabis for fun or curiosity, or with their friends, who reported the lowest average paranoia and anxiety scores.
Dr Edoardo Spinazzola, a Research Assistant at King’s IoPPN and the study’s first author said, “This research suggests that using cannabis as a mean to self-medicate physical or mental discomfort can have a negative impact on the levels of paranoia, anxiety, and depression. Most of these subgroups had average scores of depression and anxiety which were above the threshold for referral to counselling.”
Respondents were also asked to provide data on the frequency and strength of the cannabis they were using so that researchers could track their average weekly consumption of Tetrahydrocannabinol (THC) – the principle psychoactive component of cannabis.
The researchers found that the average respondent consumed 206 units of THC a week. This might equate to roughly 10-17 ‘joints’ per week, if the user was consuming an expected 20% THC content that is standard for the most common types of cannabis available in London.
However, respondents who started using cannabis to help with their anxiety, depression, or in cases where they started due to others in their household who were already using cannabis, reported on average 248, 254.7, and 286.9 average weekly THC units respectively.
Professor Tom Freeman, Director of the Addiction and Mental Health Group at the University of Bath and one of the study’s authors said, “A key finding of our study is that people who first used cannabis to manage anxiety or depression, or because a family member was using it, showed higher levels of cannabis use overall.
“In future, standard THC units could be used in a similar way to alcohol units – for example, to help people to track their cannabis consumption and better manage its effects on their health.”
In a separate study, published in Psychological Medicine, researchers explored the relationship between childhood trauma, paranoia and cannabis use.
Researchers used the same data set from the Cannabis & Me survey, with just over half of respondents (52 per cent) reporting experience of some form of trauma.
Analysis established that respondents who had been exposed to trauma as children reported higher average levels of paranoia compared to those who hadn’t, with physical and emotional abuse emerging as the strongest predictors.
Researchers also explored the relationship between childhood trauma and weekly THC consumption. Respondents who reported experience of sexual abuse had a markedly higher weekly intake of THC, closely followed by those who reported experiencing emotional and physical abuse.
Finally, the researchers confirmed that the strong association between childhood trauma and paranoia is further exacerbated by cannabis use, but is affected by the different types of trauma experienced. Respondents who said they had experienced emotional abuse or household discord were strongly associated with increased THC consumption and paranoia scores. Respondents reporting bullying, physical abuse, sexual abuse, physical neglect and emotional neglect on the other hand did not show the same effects.
Dr Giulia Trotta, a Consultant Psychiatrist and Researcher at King’s IoPPN and the study’s first author said,
“We have not only established a clear association between trauma and future paranoia, but also that cannabis use can further exacerbate the effects of this, depending on what form the trauma takes.
“Our findings will have clear implications for clinical practice as they highlight the importance of early screening for trauma exposure in individuals presenting with paranoia.”
Professor Marta Di Forti, Professor of Drug use, Genetics and Psychosis at King’s IoPPN, Clinical Lead at the South London and Maudsley NHS Foundation Trust’s Cannabis Clinic for Patients with Psychosis, and the senior author on both studies said, “There is extensive national and international debate about the legality and safety of cannabis use.
“My experience in clinic tells me that there are groups of people who start to use cannabis as a means of coping with physical and emotional pain. My research has confirmed that this is not without significant further risk to their health and wellbeing, and policy makers across the world should be mindful of the impact that legalisation , without adequate public education and health support, could have on both the individual, as well as on healthcare systems more broadly.”
Alcohol withdrawal syndrome (AWS) is a potentially life-threatening condition that may complicate patients’ recovery after surgery.
Previous studies have estimated that up to 50% of hospitalised patients with AUD will develop some degree of AWS. Up to 7% of these patients may progress to severe withdrawal, including delirium tremens (DT) that can range in severity from irritability and confusion to tremors, nausea, vomiting and seizures.
Of those patients, 16 504 (0.5%) were diagnosed with AWS, including 6591 (0.2%) with DT.
“We found that alcohol withdrawal syndrome is linked with poorer surgical outcomes, extended hospitalisations and increased costs. These findings underscore the need for standardised perioperative screening and targeted management strategies to reduce these risks,” said study lead author Timothy Pawlik, MD, PhD, professor and chair of Ohio State’s Department of Surgery.
Patients with AWS were generally younger, male and more likely to have Medicaid, according to Pawlik, who holds the Urban Meyer III and Shelley Meyer Chair for Cancer Research at The Ohio State University College of Medicine.
AWS raises the risk of postoperative complications, especially respiratory failure and sepsis. The study found that patients with AWS had longer hospital stays (median 11 vs 6 days) and higher costs ($44 300 vs $28 800).
AWS was associated with a $10 030 higher adjusted hospitalisation cost per patient undergoing surgical care, contributing to an overall excess cost of $165.6 million, said study first author Azza Sarfraz, MBBS, a surgical oncology fellow at Ohio State.
“The lack of standard screening delays early detection and intervention,” Pawlik said. “Developing strategies for early identification, inpatient withdrawal management, and perioperative risk stratification may improve surgical outcomes, lower healthcare costs, and enhance patient care.”
A new article published in the Canadian Medical Association Journal warns of the mental health dangers stemming from the increasing potency of cannabis. In Ontario, there has been a more than 14-fold increase in risk for visiting the emergency department for cannabis-related schizophrenic disorders. After a cannabis-induced psychotic episode, cessation of cannabis use is necessary to reduce the risk of relapse, and in severe cases, antipsychotics may be needed.
“Cannabis from the 2000s is not the same as in 2025,” said coauthor Dr Nicholas Fabiano, MD, resident and researcher with the Department of Psychiatry, University of Ottawa, Ottawa, Ontario. “THC content has increased by 5 times. This is likely a significant driver in the increasing link between cannabis use and schizophrenia.”
Cannabis potency is increasing — The concentration of tetrahydrocannabinol (THC) has increased fivefold in the last 20 years in Canada from about 4% to 20% in most legal dried cannabis.
High-potency and regular cannabis use is linked to increased risk of psychosis — The risk of psychosis is increased in people using high-potency THC (more than 10% THC), people using it frequently, and those who are younger and male. A history of mental disorders (depression, anxiety, etc) also appears to increase the risk.
Cannabis-induced psychosis and cannabis use disorder increase the risk of schizophrenia — A recent study of 9.8 million people in Ontario found a 14.3-fold higher risk of developing a schizophrenia-spectrum disorder in people visiting the emergency department for cannabis use and a 241.6-fold higher risk from visits for cannabis-induced psychosis.
Treatment requires stopping cannabis and taking medication — Continued use of cannabis after a first episode of cannabis-induced psychosis is linked to greater risk of returning symptoms. Antipsychotic medication can help people with severe and prolonged symptoms.
Behavioural options may help with cannabis cessation — Motivational interviewing or cognitive behavioural therapy by a physician or psychologist can help build skills to resist cravings and follow treatment recommendations.
A recent study by researchers at the University of California San Diego School of Medicine has found that individuals with cannabis use disorder (CUD) are more than three times more likely to develop oral cancer within five years compared to those without CUD. The study, published in Preventive Medicine Reports, highlights the potential long-term health risks associated with problematic cannabis use.
In 2022, 17.7 million people in the US reported daily or near-daily cannabis use. Though CUD requires a formal diagnosis and not all cannabis users develop the disorder, recent research suggests that as many as 3 in 10 cannabis users will develop CUD.
“Cannabis smoke contains many of the same carcinogenic compounds found in tobacco smoke.”
As cannabis becomes more widely available and socially accepted, it is essential to understand its potential health risks. While many consider cannabis to be safer than other drugs, such as tobacco and alcohol, there are still many unknowns about the health impacts of cannabis, particularly how the drug influences cancer risk. The new study sought to determine the relationship between CUD and oral cancer, for which tobacco smoking is known to be a significant risk factor.
“Cannabis smoke contains many of the same carcinogenic compounds found in tobacco smoke, which have known damaging effects on the epithelial tissue that lines the mouth,” said Raphael Cuomo, PhD, associate professor in the Department of Anesthesiology at UC San Diego School of Medicine and member of UC San Diego Moores Cancer Center. “These findings add to a growing body of evidence suggesting that chronic or problematic cannabis use may contribute to cancer risk in tissues exposed to combustion products.”
By analysing the electronic health records from over 45 000 patients, of whom 949 developed CUD, Cuomo found:
After adjusting for age, sex, body mass index and smoking status, people had a 325% higher likelihood of contracting oral cancer within five years compared to those without CUD.
Tobacco smokers with CUD were 624% more likely to contract oral cancer within five years compared to tobacco smokers without CUD.
Because the association between CUD and oral cancer remained even after controlling for smoking status, and because CUD was associated with greater oral cancer risk even when the analysis was restricted to smokers, the researchers hypothesise that there may be other factors underlying this risk in addition to smoke inhalation. For example, THC, the active compound in cannabis, is known to have immune-suppressing effects, which may contribute to increased cancer risk.
While more research is needed to fully explain the association between cannabis and oral cancer, the study’s results have immediate implications for cancer screening practices and public health messaging. In particular, the findings emphasise the need for further research on the long-term effects of cannabis use and the importance of integrating oral health awareness into substance use disorder treatment and counselling.
Research team finds moderate risk for preterm birth, low birth weight
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An updated systematic review finds that consuming cannabis while pregnant appears to increase the odds of preterm birth, low birth weight and infant death. This study by researchers at Oregon Health & Science University appears in JAMA Pediatrics.
Study lead author Jamie Lo, MD, MCR, is a physician-scientist who provides prenatal care for high-risk pregnancies at OHSU.
“Patients are coming to me in their prenatal visits saying, ‘I quit smoking and drinking, but is it safe to still use cannabis?’” said Lo, associate professor of obstetrics and gynaecology (maternal-foetal medicine) in the OHSU School of Medicine. “Until direct harms have been proven, they perceive it to be safe to use.”
In fact, cannabis remains one of the most common substances used in pregnancy that’s still illegal under federal law, and, unlike declines in prenatal use of alcohol or nicotine, cannabis use is continuing to increase. Lo said many of her patients are reluctant to give up cannabis during pregnancy because it helps to reduce common prenatal symptoms such as nausea, insomnia and pain.
Researchers updated the systematic review and meta-analysis, drawing on a total of 51 observational studies involving 21.1 million people to examine the potential adverse effects of cannabis use in pregnancy. The researchers found eight new studies since their previous update, raising the certainty of evidence from “very-low-to-low” to “moderate” for increased odds of low birth weight, preterm birth and babies being small for their gestational age.
The updated review also indicated increased odds of newborn mortality, though still with low certainty.
Researchers noted that the new systematic review includes a larger proportion of human observational studies examining people who only use cannabis, but don’t also use nicotine. And even though the evidence is low to moderate for adverse outcomes, Lo noted that the findings are consistent with definitive evidence in nonhuman primate models exposed to THC, the main psychoactive compound in cannabis.
The related research in animal models included standard prenatal ultrasound and MRI imaging that revealed a detrimental effect on the placenta, in terms of blood flow and availability of oxygen in addition to decreased volume of amniotic fluid.
“These findings tell me as an obstetrician that the placenta is not functioning as it normally would in pregnancy,” Lo said. “When the placenta isn’t functioning well, it can affect the baby’s development and growth.”
Even though cannabis remains a Schedule 1 substance under the federal Controlled Substances Act, Oregon is one of several states that have legalised it under state law for medicinal and recreational use. Lo said she recommends a harm-reduction approach to patients. For those who cannot abstain, she advises them to reduce the amount and frequency of use to help reduce the risk of prenatal and infant complications.
“Even using less can mitigate the risk,” she said. “Abstinence is ideal, but it’s not realistic for many patients.”
