Publisher Health

Antibiotic exposure early in life could alter human brain development in areas responsible for cognitive and emotional functions, according to a Rutgers researcher.
The laboratory study, published in the journal iScience, suggests that penicillin changes the microbiome — the trillions of beneficial microorganisms that live in and on our bodies — as well as gene expression, which allows cells to respond to its changing environment, in key areas of the developing brain. The findings suggest reducing widespread antibiotic use or using alternatives when possible to prevent neurodevelopment problems.
Penicillin and related medicines (like ampicillin and amoxicillin) are the most widely used antibiotics in children worldwide. In the United States, the average child receives nearly three courses of antibiotics before the age of 2. Similar or greater exposure rates occur in many other countries.
“Our previous work has shown that exposing young animals to antibiotics changes their metabolism and immunity. The third important development in early life involves the brain. This study is preliminary but shows a correlation between altering the microbiome and changes in the brain that should be further explored,” said lead author Martin Blaser, director of the Center for Advanced Biotechnology and Medicine at Rutgers.
The study compared mice that were exposed to low-dose penicillin in utero or immediately after birth to those that were not exposed. They found that mice given penicillin experienced substantial changes in their intestinal microbiota and had altered gene expression in the frontal cortex and amygdala, two key areas in the brain responsible for the development of memory as well as fear and stress responses.
A growing body of evidence links phenomena in the intestinal tract with signaling to the brain, a field of study known as the “gut-brain-axis.” If this pathway is disturbed, it can lead to permanent altering of the brain’s structure and function and possibly lead to neuropsychiatric or neurodegenerative disorders in later childhood or adulthood.
“Early life is a critical period for neurodevelopment,” Blaser said. “In recent decades, there has been a rise in the incidence of childhood neurodevelopmental disorders, including autism spectrum disorder, attention deficit/hyperactivity disorder and learning disabilities. Although increased awareness and diagnosis are likely contributing factors, disruptions in cerebral gene expression early in development also could be responsible.”
Future studies are needed to determine whether antibiotics directly effect brain development or if molecules from the microbiome that travel to the brain disturb gene activity and cause cognitive deficits.
The study was conducted along with Zhan Gao at Rutgers and Blaser’s former graduate student Anjelique Schulfer, as well as Angelina Volkova, Kelly Ruggles, and Stephen Ginsberg at New York University, who all played important roles in this joint Rutgers-New York University project.
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Materials provided by Rutgers University. Original written by Patti Verbanas. Note: Content may be edited for style and length.

A team led by University of Washington researchers has, for the first time, identified and classified how different people respond to the accumulation of dental plaque, the sticky biofilm that gathers on teeth. Their work, recently published in the journal Proceedings of the National Academy of Sciences (PNAS), sheds important new light on why some people may be more prone to serious conditions that lead to tooth loss and other problems.
Left unchecked, plaque buildup can induce gingivitis, or gum inflammation. Gingivitis, in turn, can lead to periodontitis, a serious gum infection that damages the soft tissue and can destroy the bone that supports teeth. Not only can this result in tooth loss, but chronic inflammation can also spur other serious health consequences, including heart disease, diabetes, cancer, arthritis, and bowel diseases.
The researchers also found a previously unidentified range of inflammatory responses to bacterial accumulation in the mouth. When bacteria build up on tooth surfaces, it generates inflammation, a tool the body uses to tamp down the buildup. Previously, there were two known major oral inflammation phenotypes, or individual traits: a high or strong clinical response and a low clinical response. The team identified a third phenotype, which they called “slow”: a delayed strong inflammatory response in the wake of the bacterial buildup.
The study revealed for the first time that subjects with low clinical response also demonstrated a low inflammatory response for a wide variety of inflammation signals. “Indeed, this study has revealed a heterogeneity in the inflammatory response to bacterial accumulation that has not been described previously,” said Dr. Richard Darveau of the UW School of Dentistry, one of the study’s authors.
His School of Dentistry colleague and study co-author Dr. Jeffrey McLean said, “We found a particular group of people that have a slower development of plaque as well as a distinct microbial community makeup prior to the start of the study.” The study authors wrote that understanding the variations in gum inflammation could help better identify people at elevated risk of periodontitis. In addition, it is possible that this variation in the inflammatory response among the human population may be related to susceptibility to other chronic bacterial-associated inflammatory conditions such as inflammatory bowel disease.
In addition, the researchers found a novel protective response by the body, triggered by plaque accumulation, that can save tissue and bone during inflammation. This mechanism, which was apparent among all three phenotypes, utilizes white blood cells known as neutrophils. In the mouth, they act something like cops on the beat, patrolling and regulating the bacterial population to maintain a stable condition known as healthy homeostasis.
In this instance, plaque is not a villain. To the contrary, the researchers said that the proper amount and makeup of plaque supports normal tissue function. Studies in mice have also shown that plaque also provides a pathway for neutrophils to migrate from the bloodstream through the gum tissue and into the crevice between the teeth and gums.
When healthy homeostasis exists and everything is working right, the neutrophils promote colonization resistance, a low-level protective inflammatory response that helps the mouth fend off an excess of unhealthy bacteria and resist infection. At the same time, the neutrophils help ensure the proper microbial composition for normal periodontal bone and tissue function.
The researchers’ findings underscore why dentists preach the virtues of regular brushing and flossing, which prevent too much plaque buildup. “The idea of oral hygiene is to in fact recolonize the tooth surface with appropriate bacteria that participate with the host inflammatory response to keep unwanted bacteria out,” Dr. Darveau said. The bacteria start repopulating the mouth’s surfaces spontaneously and almost immediately afterward, he said.

When it comes to the medicinal and therapeutic properties of Cannabis sativa, an unsolved mystery is whether there exists an “entourage effect,” whereby the pain-relieving effects of the plant as a whole are greater than any of its individual parts. New research from the University of Arizona Health Sciences has found evidence that favors the entourage effect theory and positions Cannabis terpenes, the part of the plant that provides flavor and aroma, as a promising new target for pain therapies that would require lower doses and produce fewer side effects.
“A lot of people are taking cannabis and cannabinoids for pain,” said lead researcher John Streicher, PhD, a member of the UArizona Health Sciences Comprehensive Pain and Addiction Center and associate professor of pharmacology at the College of Medicine — Tucson. “We’re interested in the concept of the entourage effect, with the idea being that maybe we can boost the modest pain-relieving efficacy of THC and not boost the psychoactive side effects, so you could have a better therapeutic.”
Terpenes are aromatic compounds found in many plants and are the basic component in essential oils. The terpene linalool, for example, gives lavender its distinctive floral scent. In addition to terpenes, Cannabis sativa contains naturally occurring compounds known as cannabinoids, the most well-known of which are cannabidiol, or CBD, and tetrahydrocannabinol, or THC, the psychoactive component of cannabis.
Researchers found that Cannabis terpenes, when used by themselves, mimic the effects of cannabinoids, including a reduction in pain sensation. When combined with cannabinoids, the pain-relieving effects were amplified without an increase in negative side effects. The paper, “Cannabis sativa terpenes are cannabimimetic and selectively enhance cannabinoid activity,” was published in Scientific Reports.
“It was unexpected, in a way,” said Dr. Streicher. “It was our initial hypothesis, but we didn’t necessarily expect terpenes, these simple compounds that are found in multiple plants, to produce cannabinoid-like effects.”
Dr. Streicher and the research team, including former graduate student and first author Justin LaVigne, PhD, former undergraduate researcher Ryan Hecksel and former postdoctoral fellow Attila Kerestztes, PhD, focused on four Cannabis terpenes: alpha-humulene, geraniol, linalool and beta-pinene. They evaluated each terpene alone and in combination with WIN55,212-2, a synthetic cannabinoid agonist that stimulates the body’s natural cannabinoid receptors.
When a cannabinoid such as THC enters the body, it binds to one of two cannabinoid receptors — CB1R, which is the most abundant, or CB2R. The receptor then activates neurons that affect physiological processes and behavior. In laboratory experiments, researchers found that all four terpenes activated the CB1R, just like THC.
Behavioral studies in mouse models revealed that when administered individually, all four terpenes lowered pain sensitivity, and at least three of the four classic cannabinoid side effects: reduced pain sensation, lowered body temperature, reduced movement and catalepsy, a freezing behavior related to the psychoactive effects of cannabinoids. When terpenes were combined with WIN55,212-2, researchers saw a greater reduction in pain sensation compared with either the terpene or WIN55,212-2 alone, demonstrating a terpene/cannabinoid interaction in controlling pain.
Dr. Streicher’s ongoing research is focusing on the use of terpenes in combination with opioids and for specific types of cancer-related pain. His long-term goal is to develop a dose-reduction strategy that uses terpenes — generally recognized as safe by the U.S. Food and Drug Administration — in combination with cannabinoids or opioids to achieve the same levels of pain relief with lower doses of drugs and fewer side effects.

Researchers from Kumamoto University, Japan have found that a component derived from turmeric essential oil, aromatic turmerone (ar-turmerone), and its derivatives act directly on dopaminergic nerves to create a neuroprotective effect on tissue cultures of a Parkinson’s disease model. This appears to be due to enhanced cellular antioxidant potency from the activation of Nrf2. The researchers believe that the ar-turmerone derivatives identified in this study can be used as new therapeutic agents for Parkinson’s disease.
Parkinson’s disease is a neurodegenerative disease caused by the selective death of dopaminergic neurons that transmit information from the substantia nigra of the midbrain to the striatum which results in decreased dopamine production. Symptoms include limb tremors, immobility, muscle rigidity, and other movement disorders. Treatments, such as dopamine supplements, are currently available but there still no way to inhibit dopaminergic neurodegeneration.
Previous studies have reported that the inflammatory response caused by the activation of microglia (cells responsible for immune function in the brain) is observed in the substantia nigra of the midbrain of Parkinson’s disease patients. Further experiments designed to mimic the in vivo state of the midbrain (midbrain slice culture) revealed that microglial activation triggers the selective degeneration of dopaminergic neurons in the substantia nigra, and that nitric oxide (NO) derived from activated microglia was involved in the neurodegeneration. These findings suggest that compounds with anti-inflammatory effects on microglia may suppress dopaminergic degeneration.
Thus, researchers analyzed aromatic tumerone (ar-turmerone), a major component of turmeric essential oil that has been reported to exhibit anti-tumor and anti-inflammatory effects on microglia. They used the BV2 microglial cell line and midbrain slice cultures to 1) determine if ar-turmerone suppresses dopaminergic neurodegeneration through its anti-inflammatory effects, and 2) identify structurally similar compounds (derivatives) that might have stronger anti-inflammatory and neuroprotective effects.
Ar-turmerone has an asymmetric carbon (S-Tur) so researchers prepared eight analogues and attempted to identify those with stronger anti-inflammatory effects. They used the inhibitory effects on the inflammatory response as induced by lipopolysaccharide (LPS)-stimulated activation of BV2 cells as an indicator. The analogues with stronger anti-inflammatory effects than S-Tur were (R)-ar-turmerone (R-Tur), ar-atlantone (Atl), and analog 2 (A2).
To examine whether these compounds, including S-Tur, have an inhibitory effect on dopaminergic degeneration, researchers then observed midbrain slice cultures in which microglial activation was induced by interferon-γ and LPS stimulation (IFN-γ/LPS). All four compounds significantly suppressed a decrease in the number of dopaminergic neurons as induced by IFN-γ/LPS. However, the production of NO, which is released from activated microglia and is involved in dopaminergic neurodegeneration, was not inhibited at all. In addition, three compounds, S-Tur, Atl and A2, inhibited dopaminergic degeneration that is induced by MPP+, a toxin that selectively damages dopaminergic neurons independent of microglial activity. These results indicate that S-Tur and its derivatives, Atl and A2, have a direct effect on dopaminergic neurons and exhibit neuroprotective effects. Furthermore, analysis using dopaminergic progenitor cell lines and midbrain slice cultures revealed that the neuroprotective effects of Atl and A2 are mediated by activation of Nrf2, a transcription factor that enhances the antioxidant potency of cells.
“Our study elucidated a new mechanism by which ar-turmerone and its derivatives directly protect mesencephalic slice dopaminergic neurons, independent of their previously reported anti-inflammatory effects on microglia,” said Associate Professor Takahiro Seki, who led the study. “We showed that two derivatives, Atl and A2, exhibit neuroprotective effects by increasing the expression of antioxidant proteins through the activation of Nrf2. In particular, the analog A2 identified in this study is a potent activator of Nrf2 and is assumed to have a strong antioxidant effect. We think it is possible that this compound may be a new dopaminergic neuroprotective agent for Parkinson’s disease treatment, and it could also be used to treat other diseases caused by oxidative stress, such as liver and kidney diseases.”
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Materials provided by Kumamoto University. Note: Content may be edited for style and length.

Heart failure hospitalizations and costs related to methamphetamine use jumped sharply over a decade in California, according to new research published today in Circulation: Cardiovascular Quality and Outcomes, an American Heart Association journal.
“Our study results should bring urgent attention to this insidious yet rapidly growing form of severe heart failure — methamphetamine-related heart failure, which is taking the lives of young people, straining health care resources and threatening to spread like wildfire in California, the West and to the rest of the nation,” said lead author Susan X. Zhao, M.D., a cardiologist at Santa Clara Valley Medical Center in San Jose, California. “California is seeing a resurgence of methamphetamine use, and the problem has been made drastically worse in recent years by the increase in purer, more potent methamphetamine throughout our communities.”
Heart failure is a chronic condition in which the heart becomes too weak to properly pump blood. Signs of heart failure include fatigue, shortness of breath and heart palpitations. According to the American Heart Association’s Heart Disease and Stroke Statistics — 2021 Update, an estimated 6 million American adults ages 20 and older have heart failure based on 2015-2018 data. The condition is most prevalent among people ages 60 and older.
Methamphetamine, also known as meth, is an addictive stimulant that can affect the cardiovascular system by triggering blood vessel spasms and life-threatening spikes in blood pressure. It can also increase plaque in the arteries and rewire the heart’s electrical system. Prolonged methamphetamine use has been associated with a severe form of dilated cardiomyopathy, a condition in which the weakened heart muscle becomes enlarged and cannot pump adequate blood. According to the 2017 U.S. National Survey on Drug Use and Health, 1.6 million people reported using methamphetamines, and the average age of new methamphetamines users was 23.
This study is a retrospective review of California hospital data including more than one million patients discharged between 2008 and 2018 with a diagnosis of heart failure. During that 11-year period, researchers noted: 42,565 (4%) of the patients had been diagnosed with methamphetamine-related heart failure — also known as MethHF — compared with 990,511 (96%) diagnosed with heart failure unrelated to methamphetamine use. Hospitalizations for methamphetamine-related heart failure rose 585%, while heart failure hospitalizations unrelated to methamphetamine use declined 6%. 94% of methamphetamine-related heart failure patients were under age 65, with more than half being between ages 35 and 54. 79% of methamphetamine-related heart failure patients were men, and nearly half of methamphetamine-related heart failure patients were white adults. Methamphetamine-related heart failure patients were also more likely to consume alcohol and use tobacco and other illicit drugs. They were more likely to be homeless compared with other heart failure patients, as well. People with methamphetamine-related heart failure had fewer pre-existing cardiovascular conditions such as atrial fibrillation or Type 2 diabetes, though, more had high blood pressure (33%) compared to heart failure patients who did not use methamphetamines (30%).Researchers found that the financial toll of methamphetamine-related heart failure is also significant: hospital stays were several days longer than those of other heart failure patients, and they had more procedures performed, leading to significantly higher health care costs. Hospitalization costs for methamphetamine-related heart failure in California rose 840%, from $41.5 million in 2008 to $390.2 million in 2018, compared with an 82% increase in costs for all heart failure-related hospitalizations, which rose from $3.5 billion to $6.3 billion.

The results of a study by an international scientific team co-led by the Translational Genomics Research Institute (TGen), an affiliate of City of Hope, suggest that — like pouring water atop a wellhead before pumping — the airway cells of patients with chronic lung diseases are “primed” for infection by the COVID-19 virus, resulting in more severe symptoms, poorer outcomes and a greater likelihood of death.
The study — published today in Nature Communications — details the genetic changes caused by chronic lung disease in the molecular makeup of a variety of cells, including the epithelial cells that line the lung and airways. The study details how those changes can help enable SARS-CoV-2, the virus that causes COVID-19, to enter the body, replicate and trigger an out-of-control immune response that fills the lungs with fluids and often results in patients needing respirators and lengthy hospitalizations.
The team used single-cell RNA sequencing technology to spell out the genetic code of 611,398 cells from various data bases, representing those with both healthy (control) lungs and those with chronic lung disease. Sequencing and analysis allowed researchers to identify molecular characteristics that may account for worse COVID-19 outcomes.
“Our results suggest that patients with chronic lung disease are molecularly primed to be more susceptible to infection by SARS-CoV-2,” said Nicholas Banovich, Ph.D., an Associate Professor in TGen’s Integrated Cancer Genomics Division, and one of the study’s senior authors. Dr. Banovich is a leading participant in the Human Cell Atlas Lung Biological Network, whose dozens of members, representing more than 80 institutions worldwide, also contributed to this study.
In addition, older-age, male-gender, smoking, and comorbidities such as high blood pressure, obesity and diabetes, are all COVID-19 risk factors that are exacerbated by chronic lung diseases, such as Chronic Obstructive Pulmonary Disease (COPD), Interstitial Lung Disease (ILD), and especially Idiopathic Pulmonary Fibrosis (IPF), a progressive scaring and stiffening of the lung tissue.
“It was recognized early in the pandemic that patients with chronic lung diseases were at particularly high risk for severe COVID-19, and our goal was to gain insight into the cellular and molecular changes responsible for this,” said Jonathan Kropski, M.D., Associate Professor of Medicine and Cell and Developmental Biology at Vanderbilt University Medical Center, and a co-senior author of the study.

A phase II study led by researchers from The University of Texas MD Anderson Cancer Center found that treatment with atezolizumab and bevacizumab was well-tolerated and resulted in a 40% objective response rate in patients with advanced malignant peritoneal mesothelioma, a rare cancer in the lining of the abdomen. Responses occurred in patients regardless of PD-L1 expression status and tumor mutation burden.
Trial results indicated that the combination was safe and effective in patients with disease progression or intolerance to previous chemotherapy treatment. The study, led by Kanwal Raghav, M.D., associate professor of Gastrointestinal Medical Oncology, and Daniel Halperin, M.D., assistant professor of Gastrointestinal Medical Oncology, was published today in Cancer Discovery.
Malignant peritoneal mesothelioma (MPeM) is known as a rare but aggressive disease with historically poor survival and limited treatment options. Because symptoms most often go unnoticed, peritoneal cancer is usually diagnosed at a late stage. If left untreated, life expectancy is often less than a year.
“There is a grave unmet need for patients with peritoneal mesothelioma,” Raghav said. “This study establishes a much-needed treatment option and represents an effort to encourage research for this rare disease.”
One of the first trials for MPeM patients
Researchers estimate that 300-500 Americans are diagnosed with MPeM each year. MPeM usually follows the same treatment as pleural mesothelioma, a cancer of the lung lining, although there are significant differences between the diseases. MPeM is far rarer, understudied, has a weaker association with asbestos exposure, affects women more frequently, occurs at a younger age and is diagnosed more often at an advanced stage.

Vaccine skepticism among young adults may stall efforts to achieve herd immunity — a threshold in which approximately 80 percent of a population is vaccinated against the coronavirus.
A study by UC San Francisco researchers found that about one in four unvaccinated people aged 18 to 25 said that they “probably will not” or “definitely will not” get the COVID-19 vaccination, despite the fact that this demographic has been found to be more likely than other age-groups to transmit coronavirus, jeopardizing the health of older unvaccinated adults and facilitating the rise of virulent vaccine variants.
The researchers analyzed March 2021 data from the Household Pulse Survey, an online nationally representative sample of the population conducted by the U.S. Census Bureau in collaboration with the National Center for Health Statistics and other agencies.
Among the 5,082 respondents, 83 percent reported that they had not been vaccinated, 10 percent said they definitely will not get the vaccine, and 14 percent said they probably will not. The study appears July 14, 2021, in the Journal of Adolescent Health.
While data from the Centers for Disease Control and Prevention (CDC) show that very few 18 to 29-year-olds die of COVID relative to older adults, this age group accounts for more than 20 percent of all COVID cases to date. Furthermore, previous research by lead author Sally Adams, PhD, RN, of the UCSF National Adolescent and Young Adult Health Information Center, found that as many as one in three young adults is at risk of severe COVID.
‘Long COVID’ May Impact Young Adults even with Mild Symptoms
“Young adults who have had COVID, regardless of symptoms, may be vulnerable to long-term complications and debilitating symptoms that may include respiratory difficulties, loss of smell and brain fog, often referred to as ‘long COVID.’ Estimates range from 10 to 50 percent for long COVID symptoms, which is a serious concern for young adults given their high infection rates and low vaccination rates,” Adams said.
“Prompt vaccinations could help limit the further development of virulent variants and infection rates among the vulnerable and unvaccinated,” she added.
Among the unvaccinated respondents who said they would definitely not or probably not get the vaccine, more than half said they were concerned about possible side effects. Half said they planned to wait and see if the vaccine was safe and may get it later. Also, within this group, a third said that they do not trust the vaccine, compared to fewer than one in 10 of those who said that they probably would get vaccinated.
The recent spate of heart inflammation cases in teens and young adults following the Pfizer and Moderna vaccines may have amplified many people’s fears, said senior author Charles Irwin Jr., MD, director of the Division of Adolescent and Young Adult Medicine at UCSF Benioff Children’s Hospitals.
“It’s important to note that the rate of heart inflammation in young people who have been vaccinated is only slightly higher than in young people who have not been vaccinated. In most cases, symptoms are mild and resolve with minimal treatment,” said Irwin. “As a result, the majority of providers support the CDC and other advisory bodies that continue to recommend the vaccine for everyone age 12 or older.”
The researchers recommend that young adults’ concerns about vaccine safety and side effects are addressed via public education campaigns. “Education and public health messaging encouraging young adult vaccination is needed, ideally harnessing social media and key influencers,” Irwin said, “including clinicians who have a key role in reducing vaccine hesitancy in youth and adult patients.”
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Materials provided by University of California – San Francisco. Original written by Suzanne Leigh. Note: Content may be edited for style and length.

A new study from the World Health Organization’s (WHO) International Agency for Research on Cancer (IARC), published in the journal Lancet Oncology, has found an association between alcohol and a substantially higher risk of several forms of cancer, including breast, colon, and oral cancers. Increased risk was evident even among light to moderate drinkers (up to two drinks a day), who represented 1 in 7 of all new cancers in 2020 and more than 100,000 cases worldwide.
In Canada, alcohol use was linked to 7,000 new cases of cancer in 2020, including 24 per cent of breast cancer cases, 20 per cent of colon cancers, 15 per cent of rectal cancers, and 13 per cent of oral and liver cancers.
“All drinking involves risk,” said study co-author Dr. Jürgen Rehm, Senior Scientist, Institute for Mental Health Policy Research and Campbell Family Mental Health Research Institute at CAMH. “And with alcohol-related cancers, all levels of consumption are associated with some risk. For example, each standard sized glass of wine per day is associated with a 6 per cent higher risk for developing female breast cancer.”
“Alcohol consumption causes a substantial burden of cancer globally,” said Dr. Isabelle Soerjomataram, Deputy Branch Head, Cancer Surveillance Branch at IARC. “Yet the impact on cancers is often unknown or overlooked, highlighting the need for implementation of effective policy and interventions to increase public awareness of the link between alcohol use and cancer risk, and decrease overall alcohol consumption to prevent the burden of alcohol-attributable cancers.”
Dr. Leslie Buckley, CAMH Chief of Addictions, added: “In our clinic we are seeing many people who report increased alcohol use since the onset of the pandemic. Although this may be related to temporary stressors, there is a potential for new habits to become more permanent. The consequences with alcohol use are often subtle harms initially that take time to show themselves, while long-term consequences such as cancer, liver disease and substance use disorder can be devastating.”
The modelling study was based on data on alcohol exposure from almost all countries of the world, both surveys and sales figures, which were combined with the latest relative risk estimates for cancer based on level of consumption.
“Alcohol causes cancer in numerous ways,” explained Dr. Kevin Shield, Independent Scientist, Institute for Mental Health Policy Research, and study co-author. “The main mechanism of how alcohol causes cancer is through impairing DNA repair. Additional pathways include chronic alcohol consumption resulting in liver cirrhosis, and alcohol leading to a dysregulation of sex hormones, leading to breast cancer. Alcohol also increases the risk of head and neck cancer for smokers as it increases the absorption of carcinogens from tobacco.”
Dr. Rehm says research into the link between light to moderate drinking and cancer is relatively new and that public policy does not yet reflect the degree of cancer risk. He added, “As an epidemiologist, I would recommend higher taxes to fully reflect the burden of disease from alcohol. Along with limiting the physical availability and marketing of alcohol, price controls are recognized as high-impact, cost-effective measures to reduce alcohol-related harm.” Governments can also consider requiring manufacturers to include information about health and safety risks associated with alcohol consumption, including cancer risk, on alcoholic beverage labels.
These suggestions and many others can be found in CAMH’s Alcohol Policy Framework. Updated in September 2019, the document proposes evidence-informed measures to effectively address the health and social harms associated with alcohol.

As Covid raged, so did the country’s other epidemic. Drug overdose deaths rose nearly 30 percent in 2020 to a […]