Smoking cannabis when you’re young may increase your risk of developing heart disease later, according to a recent University of Guelph study.
In the first study to look at specific risk indicators for cardiovascular disease (CVD) in young, healthy cannabis users, researchers found subtle but potentially important changes in heart and artery function.
Cigarette smoking is known to affect cardiovascular health, causing changes to blood vessels and the heart. Less is known about the impact of smoking cannabis on long-term CVD risk, even as use of the substance grows in Canada and abroad. Cannabis is the most commonly used recreational substance worldwide after alcohol.
“Cannabis is really widely used as a recreational substance all around the world and is becoming increasingly so,” said Christian Cheung, a PhD student in the Human Performance and Health Research Lab, part of the Department of Human Health and Nutritional Sciences (HHNS). “Scientists haven’t done that research with cannabis.”
Cheung is the lead author of the study, published recently in the Journal of Applied Physiology. His co-authors were Dr. Jamie Burr and Dr. Philip Millar, both professors in HHNS and PhD student Alexandra Coates.
The team studied 35 subjects aged 19 to 30, half of whom were cannabis users. For all subjects, they used ultrasound imaging to look at the heart and arteries. They measured arterial stiffness and arterial function, or the ability of arteries to appropriately expand with greater blood flow. All three measures are indicators of cardiovascular function and potential disease risk.

The plasticisers contained in many everyday objects can impair important brain functions in humans. Biologists from the University of Bayreuth warn of this danger in an article in Communications Biology. Their study shows that even small amounts of the plasticisers bisphenol A and bisphenol S disrupt the transmission of signals between nerve cells in the brains of fish. The researchers consider it very likely that similar interference can also occur in the brains of adult humans. They therefore call for the rapid development of alternative plasticisers that do not pose a risk to the central nervous system.
Bisphenols are plasticisers that are found in a large number of plastic products worldwide — for example, in food packaging, plastic tableware, drinking bottles, toys, tooth fillings, and babies’ dummies. In recent years, numerous health risks have already been associated with them, especially with bisphenol A (BPA). The Bayreuth research team led by Dr. Peter Machnik at the Animal Physiology research group (led by Prof. Dr. Stefan Schuster) has now for the first time investigated the effects of plasticisers on signal transmission between nerve cells in the adult brain. The study covers not only BPA, but also bisphenol S (BPS), which is often considered less harmful to health. Their findings: Both plasticisers impair communication between the nerve cells of the brain.
Permanent damage to the nervous system
The harmful effects on the brain mainly affect the delicate balance between different neuronal functions. While some brain cells transmit signals that trigger a state of excitation in downstream cells, other brain cells have the function of inhibiting downstream cells. However, the coordination of both excitation and inhibition is essential for an intact central nervous system. “It is well known that numerous disorders in the nervous system of vertebrates are triggered by the fact that excitatory signals and inhibitory signals are not or only inadequately coordinated. So, it is all the more alarming that the plasticisers BPA and BPS significantly impair precisely this coordination,” explains Dr. Peter Machnik, lead author of the study.
“We were surprised how many vital brain functions in fish are affected by the plasticisers used in numerous industries. This damage, as we were able to show, does not occur immediately. However, when the brain cells are exposed to small amounts of BPA or BPS for a month, the damage is unmistakable,” says Elisabeth Schirmer, a doctoral student from Bayreuth and first author of the study. It turns out that the plasticisers influence the action potential of brain cells. They alter the chemical and electrical transmission of signals through the synapses. In addition, they disrupt the circuits that are important for the perception and processing of acoustic and visual stimuli.
Studies on Mauthner cells in goldfish
The discovery of the damage caused by plasticisers came from detailed studies on live goldfish. The focus was on the two largest nerve cells in fish brain, the Mauthner cells. They integrate all sensory stimuli, all of which must be processed quickly and in a precisely coordinated manner when predators approach. In this case, the Mauthner cells trigger life-saving escape reactions. Due to this function, which is essential for survival, they have become particularly robust in the course of evolution. Mauthner cells are able to ward off damaging influences to a certain extent, or to compensate for damage afterwards. This makes it all the more significant that plasticisers are able to cause considerable damage to these cells.
Transferability of the results to humans — Demand for alternative plasticisers
“The findings obtained through studies on fish brains justify the assessment that BPA and BPS can also seriously damage the brains of adult humans. Against this background, it is essential that science and industry develop new plasticisers to replace these bisphenols, while being safe for human health,” says Dr. Peter Machnik. Prof. Dr. Stefan Schuster adds: “The efficiency of the research techniques we used in our study could, in addition, prove a valuable aid in the development of alternative plasticisers. They make it possible to quickly and inexpensively test how a substance under consideration affects brain cells.”
The research was funded by the German Research Foundation (DFG) as part of a Reinhart Koselleck project.
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A new source of energy expending brown fat cells has been uncovered by researchers at the Joslin Diabetes Center, which they say points towards potential new therapeutic options for obesity. According to the new report, published in Nature Metabolism on 12 March 2021, the key lies in the expression of a receptor called Trpv1 (temperature-sensitive ion channel transient receptor potential cation subfamily V member 1) — a protein known to sense noxious stimuli, including pain and temperature.
Specifically, the authors point to smooth muscle cells expressing the Trpv1 receptor and identify them as a novel source of energy-burning brown fat cells (adipocytes). This should translate into increased overall energy expenditure — and ultimately, researchers hope reduced weight.
Brown fat or brown adipose tissue is a distinct type of fat that is activated in response to cold temperatures. Its primary role is to produce heat to help maintain body temperature and it achieves that by burning calories. This has raised the prospect that such calorie burning can be translated into weight loss, particularly in the context of obesity.
“The capacity of brown and beige fat cells to burn fuel and produce heat, especially upon exposure to cold temperatures, have long made them an attractive target for treating obesity and other metabolic disorders,” said senior author Yu-Hua Tseng. “And yet, the precise origins of cold-induced brown adipocytes and mechanisms of action have remained a bit of a mystery.”
The source of these energy-burning fat cells was previously considered to be exclusively related to a population of cells that express the receptor Pdgfrα (platelet-derived growth factor receptor alpha). However, wider evidence suggests other sources may exist. Identifying these other sources would then open up potential new targets for therapy that would get around the somewhat uncomfortable use of cold temperatures to try to treat obesity.
The team initially investigated the general cellular makeup of brown adipose tissue from mice housed at different temperatures and lengths of time. Notably, they employed modern single-cell RNA sequencing approaches to try to identify all types of cells present. This avoided issues of potential bias towards one particular cell type — a weakness of previous studies, according to the authors.

Almost half of all recreational runners incur injuries, mostly relating to knees, calves or Achilles tendons, and the level of risk is equally high whatever your age, gender or running experience. These are the findings of a thesis within sport science.
Doctoral student Jonatan Jungmalm recruited a little over 200 recreational runners from the list of entrants for the Göteborgsvarvet Half Marathon and monitored them over a period of one year. To take part in the study, they had to have been running for at least a year, have run an average of at least 15 km per week over the past year and have been injury free for at least six months. The participants were men and women in the age range 18-55.
Calculation shows injury for half of runners
Over the year of the study, the recreational runners filled in a training diary, entering information about how far they ran each day and whether they felt any pain. Those who suffered sudden injury or felt pain for a prolonged period were examined by a sports doctor.
“A third of the participants were injured over the course of the study. But if you also take account of the participants who dropped out of the study, it is reasonable to assume that almost half of all recreational runners injure themselves in a year,” states Jonatan Jungmalm.
Jonatan used a particular statistical method to calculate the proportion of injured runners, taking into account the rate of dropout that is common in studies based on voluntary participation.

New research shows that people who experience big dips in blood sugar levels, several hours after eating, end up feeling hungrier and consuming hundreds more calories during the day than others.
A study published today in Nature Metabolism, from PREDICT, the largest ongoing nutritional research program in the world that looks at responses to food in real life settings, the research team from King’s College London and health science company ZOE (including scientists from Harvard Medical School, Harvard T.H. Chan School of Public Health, Massachusetts General Hospital, the University of Nottingham, Leeds University, and Lund University in Sweden) found why some people struggle to lose weight, even on calorie-controlled diets, and highlight the importance of understanding personal metabolism when it comes to diet and health.
The research team collected detailed data about blood sugar responses and other markers of health from 1,070 people after eating standardized breakfasts and freely chosen meals over a two-week period, adding up to more than 8,000 breakfasts and 70,000 meals in total. The standard breakfasts were based on muffins containing the same amount of calories but varying in composition in terms of carbohydrates, protein, fat and fibre. Participants also carried out a fasting blood sugar response test (oral glucose tolerance test), to measure how well their body processes sugar.
Participants wore stick-on continuous glucose monitors (CGMs) to measure their blood sugar levels over the entire duration of the study, as well as a wearable device to monitor activity and sleep. They also recorded levels of hunger and alertness using a phone app, along with exactly when and what they ate over the day.
Previous studies looking at blood sugar after eating have focused on the way that levels rise and fall in the first two hours after a meal, known as a blood sugar peak. However, after analyzing the data, the PREDICT team noticed that some people experienced significant ‘sugar dips’ 2-4 hours after this initial peak, where their blood sugar levels fell rapidly below baseline before coming back up.
Big dippers had a 9% increase in hunger, and waited around half an hour less, on average, before their next meal than little dippers, even though they ate exactly the same meals.

A new probe into the lingering impacts of the COVID-19 pandemic revealed correlations to six unhealthy eating behaviors, according to a study by the University of Minnesota Medical School and School of Public Health. Researchers say the most concerning finding indicates a slight increase or the re-emergence of eating disorders, which kill roughly 10,200 people every year — about one person every 52 minutes.
U of M Medical School’s Melissa Simone, PhD, a postdoctoral research fellow in the Department of Psychiatry and Behavioral Sciences, collaborated with School of Public Health professor and head of the Division of Epidemiology and Community Health, Dianne Neumark-Sztainer, PhD, MPH, to learn from study participants in Neumark-Sztainer’s Project EAT between April and May 2020.
“The COVID-19 pandemic has resulted in the rapid implementation of public health policies to reduce transmission of the virus. While these protections are necessary, the disruptions to daily life associated with the ongoing pandemic may have significant negative consequences for the risk of eating disorders and symptoms,” said Simone, who is the lead author of the study. “Eating disorders have one of the highest mortality rates across all psychiatric health concerns, and therefore, it is important to try to make links between the consequences of the pandemic and disordered eating behaviors.
The study aimed to understand potential associations between stress, psychological distress, financial difficulties and changes in eating behaviors during the COVID-19 pandemic through the analysis of both qualitative and quantitative data. Simone’s findings, published in the International Journal of Eating Disorders, found six key themes of eating behavior changes: Mindless eating and snacking; Increased food consumption; Generalized decrease in appetite or dietary intake; Eating to cope; Pandemic-related reductions in dietary intake; And, a re-emergence or marked increase in eating disorder symptoms.Approximately 8% of those studied reported extreme unhealthy weight control behaviors, 53% had less extreme unhealthy weight control behaviors and 14% reported binge eating. The study revealed that these outcomes were significantly associated with poorer stress management, greater depressive symptoms and moderate or extreme financial difficulties.
“There has been a lot of focus on obesity and its connection with COVID-19. It is also important to focus on the large number of people who have been engaging in disordered eating and are at risk for eating disorders during and following the pandemic,” said Neumark-Sztainer, who is the principal investigator of Project EAT. “The majority of the young adults in our study are from diverse ethnic/racial and lower income backgrounds, who often do not receive the services they need. To ensure health inequities do not increase, we need to meet the needs of these populations.”
Simone added, “The economic consequences of the COVID-19 pandemic will likely persist long beyond the dissemination of a vaccine. Because our findings suggest that moderate or severe financial difficulties may be linked with disordered eating behaviors, it is essential that eating disorder preventive interventions and treatment efforts be affordable, easily accessible and widely disseminated to those at heightened risk. As such, online or mobile-based interventions may prove to be effective and accessible modes for targeted intervention efforts.”
This study was funded by the National Heart, Lung, and Blood Institute (R01HL116892, R35HL139853: Principal Investigator: D. Neumark-Sztainer), the National Center for Advancing Translational Sciences (TL1R002493, UL1TR002494), and the National Institute of Mental Health (T32MH082761).
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Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder worldwide, affecting as much as a quarter of humanity. It is characterized by fat accumulation in liver cells and may progress to inflammation, cirrhosis and liver failure. Now, researchers at the University of Tsukuba reveal the positive effects, beyond the expected weight-loss benefit, of exercise on the liver.
NAFLD is associated with unhealthy behaviors such as overeating and a sedentary lifestyle. In Japan 41% of middle-aged men have NAFLD and 25% will progress to non-alcoholic steatohepatitis (NASH) and hepatic dysfunction.
Weight reduction is fundamental to NAFLD management. Unfortunately, achieving a targeted bodyweight without supervision is difficult, and maintaining this over time even more so. Hitherto, exercise was considered adjunctive to dietary restrictions for weight loss but the other benefits such as reduced hepatic steatosis (fatty change) and stiffness are being increasingly recognized. However, the underlying mechanisms remain unclear.
“We compared data from obese Japanese men with NAFLD on a 3-month exercise regimen with those on dietary restriction targeting weight loss,” senior author Professor Junichi Shoda explains. “We tracked hepatic parameters, reduction in adipose tissue, increase in muscle strength, reductions in inflammation and oxidative stress, changes in organokine concentrations, and expression of target genes of Nrf2, an oxidative stress sensor.”
The researchers found that exercise preserved muscle mass better, though with modest decrease of body and fat mass. Remarkably, ultrasound elastography revealed that the exercise regimen reduced liver steatosis by an additional 9.5%, liver stiffness by an additional 6.8%, and the FibroScan-AST Score (a measure of liver fibrosis) by an additional 16.4% over the weight-loss regimen.
Additionally, the exercise regimen altered the circulating concentrations of specific organokines and apparently induced anti-inflammatory and anti-oxidative stress responses through activation of the Nrf2 (nuclear factor E2-related factor 2), an oxidative stress sensor. It also enhanced the phagocytic capacity of Kupffer cells which help maintain liver function.
Professor Shoda explains the relevance of their findings. “Our research shows how exercise prevents liver steatosis and fibrosis in NAFLD and clarifies that this benefit is compounded by preservation of muscle mass and is independent of weight changes. Patients on exercise regimens may become demotivated and drop out if they do not experience significant weight loss. Therefore, moderate to vigorous intensity exercise should be integrated in all NAFLD therapeutic regimens, and patients at risk for NASH should be encouraged to persevere with moderate to high intensity exercise regardless of whether or not they lose weight.”
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Humans cannot live on protein alone — even for the ancient indigenous people of the Pacific Northwest whose diet was once thought to be almost all salmon.
In a new paper led by Washington State University anthropologist Shannon Tushingham, researchers document the many dietary solutions ancient Pacific Coast people in North America likely employed to avoid “salmon starvation,” a toxic and potentially fatal condition brought on by eating too much lean protein.
“Salmon was a critical resource for thousands of years throughout the Pacific Rim, but there were a lot of foods that were important,” said Tushingham the lead author of the paper published online on April 8 in the American Journal of Physical Anthropology. “Native people were not just eating salmon. There’s a bigger picture.”
Some archeologists have contended for years that prehistoric Northwest people had an “extreme salmon specialization,” a theory primarily based on the amount of salmon bone found at archeological sites.
Tushingham and her co-authors argue that such a protein-intensive diet would be unsustainable. They point to nutritional studies and a global database of hunter-gatherer diets that indicate people have dietary limit on lean protein of around 35%. While it can vary by individual, exceeding that ceiling can be physically debilitating within a few days and fatal within weeks. Early explorers in the U.S. West subsisting on lean wild game discovered this problem the hard way and called it “rabbit starvation” or “caribou sickness.”
This toxic situation can apply to any lean meat, including salmon, Tushingham said. To avoid “salmon starvation,” early Pacific Coast people had to find ways to get other nutrients, especially for children and nursing mothers who have even lower dietary thresholds for lean protein.
“There were ingenious nutritional and cultural solutions to the circumstances in the Northwest,” said Tushingham. “Yes, salmon was important, but it wasn’t that simple. It wasn’t just a matter of going fishing and getting everything they needed. They also had to think about balancing their diet and making sure everybody could make it through the winter.”
The researchers point to evidence in California that people offset stored salmon protein with acorns; in Oregon and Washington, they ate root crops like camas as well as more fat-heavy fish such as eulachon. Further north, where plants are more limited, communities often ate marine mammals with high fat content such as seals and walrus. In far north interior, where there are few plants and the salmon runs can go thousands of miles inland, this was particularly challenging. Lean dried salmon was an important food source, and people circumvented salmon starvation through trading for oil with coastal peoples or obtaining fat through processing bone marrow from caribou and elk.
The authors focus on the limits of salmon, which used to be considered a “prime mover” of Pacific Northwest populations, but their analysis also has implications for the study of historical human nutrition. If their argument is correct, it is unlikely that any human society was fully driven by pursuit of protein alone as their diets had to be more complex.
“People try to come up with one ‘paleo-diet,’ but there was no one specific ideal diet,” said Tushingham. There were nutritional baselines that they had to cover, and nutritional limits that they couldn’t exceed. There were many good solutions. It depended on where you lived and the history of your community.”
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Materials provided by Washington State University. Original written by Sara Zaske. Note: Content may be edited for style and length.

Humans are exposed to many types of bacteria daily, the majority of which are harmless. However, some bacteria are pathogenic, which means they can cause disease. An extremely common pathogenic bacterial infection is Helicobacter pylori (H. pylori) in the stomach, where it can lead to chronic inflammation (gastritis), ulcers, and even cancer. A group of researchers from Osaka University have determined a specific molecular mechanism that H. pylori uses to adapt to growing in the human stomach for long periods of time.
In a report published in Nature Communications, this group found that a small RNA molecule called HPnc4160 plays a key role in how H. pylori invades the stomach and leads to disease.
Previous studies showed that HPnc4160 is conserved in different strains of H. pylori, suggesting that it has an important function. Yet, the amount of this molecule produced in the bacteria is variable among strains. Genetic analysis revealed that a specific part of the H. pylori gene, called the T-repeat region, varied in length from strain to strain. The researchers became interested in how this region affected HPnc4160 expression. Additionally, they were curious how these fluctuations would allow some strains to colonize the human stomach more efficiently than others.
“Slight differences in the genetic sequence of H. pylori can sometimes give certain strains advantages over others that allow it to grow better,” says lead author of the study Ryo Kinoshita-Daitoku. “We were interested in the genetic and molecular reasons behind why particular strains are more pathogenic and can live in the stomach for decades, leading to cancer development.”
To address these questions, the researchers infected gerbils and mice with wild type (normal) H. pylori for 8 weeks, then extracted and genetically characterized the mutant strains that appeared. They discovered that strains with a higher number of T-repeats had lower expression of HPnc4160.
“We found that the H. pylori strains with low HPnc4160 levels were more infectious,” explains Hitomi Mimuro, senior author. “When this RNA was completely absent, the amounts of several bacterial pathogenic factors significantly increased and the strain showed stronger colonization within the rodent stomach.”
One of the pathogenic factors was the bacterial protein CagA, which is known as an oncoprotein because it can promote cancer development.
“Interestingly, we observed longer T-repeat regions, lower levels of HPnc4160, and higher levels of CagA in gastric cancer patients compared with those not suffering from cancer,” describes Kinoshita-Daitoku.
These novel findings provide crucial information regarding the molecular and genetic landscape of highly pathogenic H. pylori and may assist in the development of innovative therapeutics for the treatment of H. pylori related illnesses, including gastric cancer.
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Researchers at the University of Calgary and The Hospital for Sick Children (SickKids), in Toronto, have discovered genetic risk factors for OCD that could help pave the way for earlier diagnosis and improved treatment for children and youth.
“Our group made the first finding of a genome-wide significant risk gene relevant to childhood OCD,” says Dr. Paul Arnold, MD, PhD, co-principal investigator, a professor and director of The Mathison Centre for Mental Health Research & Education at the Cumming School of Medicine. “We’ve known that OCD runs in families, but we hadn’t identified and validated specific genetic risks of OCD symptoms in children and youth until now.”
The research drew on the Spit for Science study, a research project led by SickKids looking at how genes interact with the environment to impact physical and mental health. Participants from the community were recruited via an innovative research design run out of the Ontario Science Centre, which has generated a diverse sample of 23,000 participants thus far. Participants provide a DNA sample through their saliva, do a cognitive task, and complete questionnaires on their health, lifestyle and behaviours.
In this study, saliva samples from over 5,000 children and youth were scanned and compared to participant responses using the Toronto Obsessive-Compulsive Scale (TOCS). The TOCS is a questionnaire used to evaluate obsessive-compulsive traits developed by Dr. Arnold and the team at SickKids. After looking across millions of genetic variants from the saliva samples, the team identified that children and youth with a genetic variant in the gene PTPRD had a greater risk for more obsessive-compulsive traits. The findings are published in Translational Psychiatry.
“Discovering the genes involved in OCD is critical to help improve patients’ lives. It is still early days, but our hope is these findings will lead us to understand the causes of OCD, which in turn could help identify people with OCD sooner and develop better treatments,” says Dr. Christie Burton, PhD, lead author and research associate in the Neurosciences & Mental Health program at SickKids.
The research team, which also includes co-principal investigators, Drs. Jennifer Crosbie, PhD, Clinical Psychologist at SickKids, and Russell Schachar, MD, Psychiatrist at SickKids, highlight that a greater understanding of the underlying genetics may eventually be an important complement to clinical assessment and could help guide treatment options in the future.
“OCD can present very differently and at various ages in each individual, adding to the challenge of treatment and diagnosis,” says Crosbie, who is also an associate scientist in the Neurosciences & Mental Health program at SickKids. “Studies like this one are an important step towards developing precision medicine approaches for mental health.”
Sam, 17, lives with OCD and with therapy and medication, he says he has been able to face his obsessions and compulsions, ride out the anxiety and control his actions. Looking back at his childhood, Sam says he had some OCD tendencies as early as elementary school, but neither he nor his family realized he had a mental illness. The researchers hope that by understanding the genetics of OCD they can develop better treatments, improve outcomes and diagnose youth like Sam earlier.
“At first I wasn’t sure what to do with the diagnosis, it was very foreign, I didn’t want to perceive myself as having a mental health issue,” says Sam. “But, knowing I have OCD helped me overcome the challenges. With therapy and medication, I’ve stopped OCD from overtaking my life and taken back control.”
Sam is a real teenager, but Sam isn’t his real name. He says due to the stigma around OCD he would prefer to remain anonymous.
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Materials provided by University of Calgary. Original written by Kelly Johnston. Note: Content may be edited for style and length.