New research from investigators at Mass General Brigham suggests that a commonly used type 2 diabetes medication is linked to a higher rate of heart-related conditions compared to medications that hit other targets. The study examined nationwide data from nearly 50,000 patients treated with different sulfonylureas and found that glipizide – the most widely used drug in the US within this category, but not available in South Africa – was linked to higher incidence of heart failure, related hospitalisation and death compared to dipeptidyl peptidase-4 (DPP-4) inhibitors. Results are published in JAMA Network Open.
“Patients with type 2 diabetes are at heightened risk of adverse cardiovascular incidents such as stroke and cardiac arrest,” said corresponding author Alexander Turchin, MD, MS, of the Division of Endocrinology at Brigham and Women’s Hospital (BWH), a founding member of the Mass General Brigham healthcare system. “While sulfonylureas are popular and affordable diabetes medications, there is a lack of long-term clinical data on how they affect cardiac health in comparison to more neutral alternatives like dipeptidyl peptidase 4 inhibitors.”
Turchin and co-authors emulated a target trial by analysing electronic health records and insurance claims data from the BESTMED consortium. The cohort included 48 165 patients with type 2 diabetes and moderate cardiovascular risk who received care at 10 different study sites across the country, including BWH, as well as those covered by two different national health insurance plans.
The researchers studied the five-year risk of major adverse cardiovascular events in patients treated with different sulfonylureas (glimepiride, glipizide or glyburide) or DPP4i in addition to metformin, a primary diabetes medication. They found that glipizide was associated with a 13% increase in cardiovascular risk when compared to DPP4i, while glimepiride and glyburide led to relatively smaller and less clear effects, respectively. The authors propose that further research is needed to uncover the underlying mechanisms.
“Our study underscores the importance of evaluating each drug in a particular pharmacological class on its own merits,” said Turchin.
While the incidence of breast cancer is highest for white women, Black women are more likely to have early-onset or more aggressive subtypes of breast cancer, such as triple-negative breast cancer. Among women under 50, the disparity is even greater: young Black women have double the mortality rate of young white women.
Now, research from the University of Notre Dame is shedding light on biological factors that may play a role in this disparity. The study published in iScience found that a population of cells in breast tissues, dubbed PZP cells, send cues that prompt behavioural changes that could promote breast cancer growth.
Funded by the National Cancer Institute at the National Institutes of Health, the study set out to explore what biological differences in breast tissue could be related to early onset or aggressive breast cancers. Most breast cancers are carcinomas, or a type of cancer that develops from epithelial cells. In healthy tissue, epithelial cells form linings in the body and typically have strong adhesive properties and do not move.
The researchers focused on PZP cells as previous studies had shown that these cells are naturally and significantly higher in healthy breast tissues of women of African ancestry than in healthy breast tissues of women of European ancestry. While PZP cell levels are known to be elevated in breast cancer patients in general, their higher numbers in healthy, African ancestry tissues could hold clues to why early-onset or aggressive breast cancers are more likely to occur in Black women.
“The disparity in breast cancer mortality rates, particularly among women of African descent, is multifaceted. While socioeconomic factors and delayed diagnosis may be contributing factors, substantial emerging evidence suggests that biological and genetic differences between racial groups can also play a role,” said Crislyn D’Souza-Schorey, the Morris Pollard Professor of Biological Sciences at Notre Dame and corresponding author of the study.
The study showed how PZP cells produce factors that activate epithelial cells to become invasive, where they detach from their primary site and invade the surrounding tissue.
For example, a particular biological signaling protein known as AKT is often overactive in breast cancers. This study showed that PZP cells can activate the AKT protein in breast epithelial cells, which in part allows them to invade the surrounding environment. PZP cells also secrete and deposit certain proteins outside the cell that guide the movement of breast epithelial cells as they invade.
Overall, the results of the study emphasize multiple mechanisms by which PZP cells may influence the early stages of breast cancer progression and their potential contribution to disease burden.
The researchers also looked at how a targeted breast cancer drug, capivasertib, which inhibits the AKT protein, impacted PZP cells and found it markedly reduced the effects of the PZP cells on breast epithelial cells.
“It’s important to understand the biological and genetic differences within normal tissue as well as tumours among racial groups, as these variations could potentially influence treatment options and survival rates. And consequently, in planning biomarker studies, cancer screenings or clinical trials, inclusivity is important,” said D’Souza-Schorey, also an affiliate of Notre Dame’s Berthiaume Institute for Precision Health and Harper Cancer Research Institute.
Genetic ancestry is much more complicated than how people report their race and ethnicity. New research, using data from the National Institutes of Health’s (NIH) All of Us Research Program, finds that people who identify as being from the same race or ethnic group can have a wide range of genetic differences. The findings are reported in the American Journal of Human Genetics, a Cell Press journal.
As doctors and researchers learn more about how genetic variants influence the incidence and course of human diseases, the study of genetic ancestry has become increasingly important. This research is driving the field of precision medicine, which aims to develop individualised healthcare.
People whose ancestors came from the same part of the world are likely to have inherited the same genetic variants, but self-identified race and ethnicity don’t tell the whole story about a person’s ancestors. NIH’s All of Us Research Program was created in part to address this puzzle and to learn more about how genetic ancestry influences human health.
In the current study, the investigators looked at the DNA of more than 230 000 people who have volunteered to share their health information for All of Us. They compared it to other large DNA projects from around the world using a technique called principal component analysis (PCA) to visualize population structure and help identify genetic similarity between individuals and groups of people. This analysis showed that people in the US have very mixed ancestry, and their DNA doesn’t always match the race or ethnicity they write on forms. Instead of falling into clear groups based on race or ethnicity, people’s genetic backgrounds show gradients of variation across different US regions and states.
This is especially significant for people who identify as being of Hispanic or Latino origin. These people have a wide-ranging blend of ancestries from European, Native American, and African groups. Importantly, genetic ancestry among these people varies across the US in part because of historic migration patterns. For example, Hispanics/Latinos in the Northeast are more likely to have Caribbean (and thus African) ancestry, and those in the Southwest are more likely to have Mexican and Central American (and thus Native American) ancestry.
One specific discovery was that ancestry was significantly associated with body mass index (BMI) and height, even after adjusting for socio-economic differences. For example, West and Central African ancestries were associated with higher BMI, whereas East Africa ancestry was associated with lower BMI. There were similar findings showing that people with ancestral origins from different parts of Europe have different body measurements including height, with northern European ancestry associated with greater height and southern European ancestry associated with shorter height. This suggests that subcontinental differences in ancestry can have opposite effects on biological traits and diseases.
This finding suggests that the subcontinental differences in ancestry between individuals can have opposite effects on biological traits, diseases, and health outcomes, emphasizing the importance of not classifying individuals into broad ancestry groups such as African, European, or Asian. Doing this will help to make this research more accurate and will help to improve the field of precision medicine.
Children born to obese mothers are at higher risk of developing metabolic disorders, even if they follow a healthy diet themselves. A new study from the University of Bonn published in the journal Nature offers an explanation for this phenomenon. In obese mice, certain cells in the embryo’s liver are reprogrammed during pregnancy. This leads to long-term changes in the offspring’s metabolism. The researchers believe that these findings could also be relevant for humans.
The team focused on the so-called Kupffer cells. These are macrophages that help protect the body as part of the innate immune system. During embryonic development, they migrate into the liver, where they take up permanent residence. There, they fight off pathogens and break down ageing or damaged cells.
“But these Kupffer cells also act as conductors,” explains Prof Dr Elvira Mass from the LIMES Institute at the University of Bonn. “They instruct the surrounding liver cells on what to do. In this way, they help ensure that the liver, as a central metabolic organ, performs its many tasks correctly.”
Changing the tune: From Beethoven to Vivaldi
It appears, however, that it is this conducting function that is changed by obesity. This is what mouse experiments carried out by Mass in cooperation with other research groups at the University of Bonn suggest. “We were able to show that the offspring of obese mothers frequently developed a fatty liver shortly after birth,” says Dr Hao Huang from Mass’s lab. “And this happened even when the young animals were fed a completely normal diet.”
The cause of this disorder seems to be a kind of “reprogramming” of the Kupffer cells in the offspring. As a result, they send out molecular signals that instruct the liver cells to take up more fat. Figuratively speaking, they no longer conduct one of Beethoven’s symphonies but rather a piece by Vivaldi.
This shift already seems to occur during embryonic development and is triggered by metabolic products from the mother. These activate a kind of metabolic switch in the Kupffer cells and change the way these cells direct liver cells in the long term. “This switch is a so-called transcription factor,” says Mass. “It controls which genes are active in Kupffer cells.”
No fatty liver without the molecular switch
When the researchers genetically removed this switch in the Kupffer cells during pregnancy, the offspring did not develop a fatty liver. Whether this mechanism could also be targeted with medication is still unclear. The teams now plan to investigate this in follow-up studies.
If new treatment approaches emerge from this, it would be good news. The altered behaviour of the Kupffer cells likely has many negative consequences. Fat accumulation in the liver, for example, is accompanied by strong inflammatory responses. These can cause increasing numbers of hepatocytes to die and be replaced with scar tissue, resulting in fibrosis. At the same time, the risk that hepatocytes degenerate and become cancerous increases.
“It is becoming ever more evident that many diseases in humans already begin at a very early developmental stage,” says Mass, who is also spokesperson for the transdisciplinary research area “Life & Health” and a board member of the “ImmunoSensation2” Cluster of Excellence at the University of Bonn. “Our study is one of the few to explain in detail how this early programming can happen.”
Consuming certain sweeteners commonly found in foods and beverages may increase the risk of early puberty in children, particularly among those who are genetically predisposed, according to a study being presented Sunday at ENDO 2025, the Endocrine Society’s annual meeting in San Francisco, Calif.
The researchers found that consuming aspartame, sucralose, glycyrrhizin and added sugars was significantly associated with a higher risk of early puberty, especially in children with certain genetic traits. The more of these sweeteners the teens consumed, the higher their risk of central precocious puberty.
“This study is one of the first to connect modern dietary habits – specifically sweetener intake – with both genetic factors and early puberty development in a large, real-world cohort,” said Yang-Ching Chen, MD, PhD, of Taipei Municipal Wan Fang Hospital and Taipei Medical University in Taipei, Taiwan. “It also highlights gender differences in how sweeteners affect boys and girls, adding an important layer to our understanding of individualised health risks.”
A type of early puberty known as central precocious puberty is increasingly common. It can lead to emotional distress, shorter adult height, and increased risk of future metabolic and reproductive disorders.
Chen’s previous research found that certain sweeteners can directly influence hormones and gut bacteria linked to early puberty. For example, one artificial sweetener, acesulfame potassium or AceK, was shown to trigger the release of puberty-related hormones by activating “sweet taste” pathways in brain cells and increasing stress-related molecules. Another sweetener, glycyrrhizin (found in liquorice) was found to change the balance of gut bacteria and reduce the activity of genes involved in triggering puberty.
“This suggests that what children eat and drink, especially products with sweeteners, may have a surprising and powerful impact on their development,” Chen said.
The new findings come from the Taiwan Pubertal Longitudinal Study (TPLS), begun in 2018. The study included data from 1407 teens. Central precocious puberty was diagnosed in 481 teens. The researchers assessed teens’ sweetener intake through validated questionnaires and testing of urine samples. Genetic predisposition was quantified using polygenic risk scores derived from 19 genes related to central precocious puberty. Early puberty was diagnosed based on medical exams, hormone levels and scans.
Sucralose consumption was linked to a higher risk of central precocious puberty in boys and consumption of glycyrrhizin, sucralose and added sugars was associated with a higher risk of central precocious puberty in girls.
“The findings are directly relevant to families, paediatricians and public health authorities,” Chen said. “They suggest that screening for genetic risk and moderating sweetener intake could help prevent early puberty and its long-term health consequences. This could lead to new dietary guidelines or risk assessment tools for children, supporting healthier development.”
PFAS lurks in numerous consumer products – from nonstick cookware and food packaging to stain-resistant fabrics and personal care items. Photo by Cooker King on Unsplash
New research reveals that tiny amounts of per- and polyfluoroalkyl substances (PFAS; widely known as “forever chemicals”) cross the placenta and breast milk to alter infants’ developing immune systems, potentially leaving lasting imprints on their ability to fight disease.
University of Rochester Medical Center (URMC) researchers tracked 200 local healthy mother–baby pairs, measuring common PFAS compounds in maternal blood during pregnancy and then profiling infants’ key T‑cell populations at birth, six months, and one year. By age 12 months, babies whose mothers had higher prenatal PFAS exposure exhibited significantly fewer T follicular helper (Tfh) cells – vital coaches that help B cells produce strong, long‑lasting antibodies – and disproportionately more Th2, Th1, and regulatory T cells (Tregs), each linked to allergies, autoimmunity, or immune suppression when out of balance.
“This is the first study to identify changes in specific immune cells that are in the process of developing at the time of PFAS exposure,” said Kristin Scheible, MD, an associate professor of Pediatrics and Microbiology & Immunology at URMC and lead author of the study, which appears in the journal Environmental Health Perspectives. “Identification of these particular cells and pathways opens up the potential for early monitoring or mitigation strategies for the effects of PFAS exposure, in order to prevent lifelong diseases.”
Implications for vaccines, allergies, and autoimmunity
Tfh cell depletion helps explain previous findings that higher PFAS levels in children correlate with weaker vaccine responses to tetanus, measles, and other routine immunisations. Conversely, the uptick in Th2 and Treg cells can predispose to allergic inflammation or dampened defences, while excess Th1 activity raises concerns about future autoimmune conditions such as juvenile arthritis or type 1 diabetes.
“The cells impacted by PFAS exposure play important roles in fighting infections and establishing long-term memory to vaccines,” said Darline Castro Meléndez, PhD, a researcher in Scheible’s lab and first author of the study. “An imbalance at a time when the immune system is learning how and when to respond can lead to a higher risk of recurrent infections with more severe symptoms that could carry on through their lifetime.”
Minimising PFAS exposure
Although Rochester’s drinking water meets current safety standards, PFAS lurks in numerous consumer products – from nonstick cookware and food packaging to stain-resistant fabrics and personal care items. The study’s mothers had relatively low PFAS blood levels compared to other regions, yet the immune shifts were pronounced even in this small sample.
While not all environmental exposures can be avoided, families can reduce PFAS contact during critical windows of foetal and infant immune development. “Use water filters, minimise cooking in damaged nonstick pans, switch to alternatives like stainless steel or cast iron, and store food in glass or ceramic containers,” said Scheible. “Small steps can help lower the cumulative burden of exposure.”
The team plans a longer follow-up to determine whether these early T‑cell imbalances persist into toddlerhood and whether they translate into more infections, allergies, or autoimmune diseases. Measuring PFAS in infants directly and unravelling the molecular underpinnings of these immune disruptions are key objectives for future research.
A new study has found that the bone fracture protection women get from menopausal hormone therapy (MHT, also known as HRT) disappears within a year of stopping treatment.
In the new study, published in Lancet Healthy Longevity, experts from the School of Medicine at the University of Nottingham, also found that in most cases, stopping treatment is then followed by some years of elevated fracture risk compared to women who have never used MHT. Fracture risks then falls to be similar to, and then lower than women who have never used MHT.
The study was funded by the National Institute for Health and Care Research (NIHR) SPCR.
During menopause, all women experience a drop in hormone levels, particularly of oestrogen. This can cause a range of distressing mental and physical side effects, requiring use of MHT. However, oestrogen deficiency in women also leads to increased age-related bone weakening. Previous studies have confirmed a protective role of the oestrogen component in MHT treatments, and MHT is known to decrease fracture risk when it is being used.
However, MHT is also associated with increased risk of breast cancer and blood clots, so long-term MHT use is not recommended. For women using MHT to counteract increasing bone fragility, it is, therefore, important to know the strength and persistence of any protective effect after stopping treatment. Detailed information on this aspect from past studies has been unclear – covering only the first couple of years, and also being somewhat conflicting.
In this new study, experts used data for 6 000 000 women from around 2000 GP surgeries in the UK, which allowed them to follow-up of fracture risk levels for up to 25 years. The researchers identified all women with records of first fracture (cases) and matched each to a number of women of the same age and from the same practice, but without record of fracture (controls). They then compared the MHT use in cases before their fracture with the MHT use among their matched controls.
The findings of our study confirmed that women on MHT show a progressively reducing fracture risk compared with women not using MHT. More importantly, we also observed a clear pattern of risk change after therapy was discontinued. For most women, the bone protective effect of MHT use disappears completely within about one year of treatment being stopped, then their fracture risk rises compared to never users, peaking after about three years, before declining to become again equivalent to never users – about 10 years after discontinuation – and then again continuing to decline relative to never users. So, even after stopping MHT, women should benefit from notably reduced fracture risk in their later decades.”
Dr Yana Vinogradova, from the Centre for Academic Primary Care in the School of Medicine, and lead author of the study
This observed risk pattern was the same for all menopausal hormonal treatments, but the level of excess risk depended on the treatment type and the length of past MHT use.
“Our comparative illustration of observed patterns of fracture risk for short and long use can help doctors and patients when discussing MHT treatment options, and to consider how fracture risk may change after stopping MHT use. Anticipating periods of increased risk might prompt doctors to check patients’ bone health at discontinuation, particularly for patients most at risk with other fracture risk factors such as smoking or inactivity.
“These novel findings may also usefully stimulate further clinical and biological research into these treatments,” adds Dr Vinogradova.
A collaborative new study involving KEMRI-Wellcome Trust researchers has highlighted a new way to control malaria transmission. The study found that ivermectin, a drug normally used for neglected tropical diseases, led to a 26% reduction in new malaria infections among children aged 5-15 by killing feeding mosquitoes.
Malaria remains a global health challenge, with 263 million cases and 597 000 deaths reported in 2023. Current vector control methods, such as long-lasting insecticidal nets and indoor residual spraying, have become less effective due to insecticide resistance and behavioural adaptations in mosquitoes to bite outdoors and during dusk or dawn, when people are not protected by these measures. This underscores the urgent need for innovative solutions to combat malaria.
The BOHEMIA trial, the largest study on ivermectin for malaria to date, showed a 26% reduction in new malaria infection on top of existing bed nets,providing strong evidence of ivermectin’s potential as a complementary tool in malaria control. Coordinated by the Barcelona Institute for Global Health (ISGlobal) – an institution supported by the “la Caixa” Foundation – in collaboration with the Manhiça Health Research Centre and the KEMRI-Wellcome Trust Research Programme, the study has been published in The New England Journal of Medicine.
Ivermectin is a drug traditionally used to treat neglected tropical diseases like onchocerciasis which causes river blindness and lymphatic filariasis which causes elephantiasis. It has now been shown to reduce malaria transmission by killing the mosquitoes that feed on treated individuals. Given the rising resistance to conventional insecticides, ivermectin could offer an effective new approach totackle malaria transmission, especially in regions where traditional methods have become less effective.
The Unitaid-funded BOHEMIA project (Broad One Health Endectocide-based Malaria Intervention in Africa) conducted two Mass Drug Administration (MDA) trials in the high-burden malaria regions: Kwale County (Kenya) and Mopeia district (Mozambique). The trials assessed the safety and efficacy of a single monthly dose of ivermectin (400mcg/kg) given for three consecutive months at the start of the rainy season in reducing malaria transmission. In Kenya, the intervention targeted children aged 5–15, while in Mozambique it focused on children under five.
In Kwale County, Kenya, children who received ivermectin experienced a 26% reduction in malaria infection incidence compared to those who received the control drug. The trial involved over 20 000 participants and more than 56 000 treatments, demonstrating that ivermectin significantly reduced malaria infection rates – particularly among children living further from cluster borders or in areas where drug distribution was more efficient. Moreover, the safety profile of ivermectin was favourable, with no severe drug-related adverse events and only mild, transient side effects already seen with ivermectin in campaigns against neglected tropical diseases.
Dr Joseph Mwangangi, Senior Principal Research Scientist at the KEMRI-Wellcome Trust Research Programme, added: ‘These results align with the World Health Organization’s (WHO) criteria for new vector control tools.’
Carlos Chaccour, co-principal investigator of the BOHEMIA project said: ‘We are thrilled with these results. Ivermectin has shown great promise in reducing malaria transmission and could complement existing control measures. With continued research, ivermectin MDA could become an effective tool for malaria control and even contribute to elimination efforts.’
In contrast, the implementation of the Mozambique trial in the rural district of Mopeia faced severe disruptions due to Cyclone Gombe in 2022 and a subsequent cholera outbreak, which significantly disrupted operations.
Francisco Saúte, director of the Manhiça Health Research Centre said: ‘One of the most important lessons we learned from the trial in Mopeia is thatstrong community engagement is essential. Building trust with local communities and fostering close collaboration with the Health Ministry, National Malaria Control Program, and local authorities was key to ensuring acceptance of the ivermectin MDA.’
In addition to reducing malaria transmission, ivermectin MDA offers significant collateral benefits. The BOHEMIA team found an important reduction in the prevalence of skin infestations such as scabies and head lice in the ivermectin group in Mozambique, and the community reported a major reduction in bed bugs in Kenya. These effects are particularly valuable when ivermectin is integrated into existing delivery systems, maximising its impact on public health.
The study is part of a larger global effort to assess ivermectin’s potential in malaria control. The findings have been reviewed by the WHO vector control advisory group, which concluded that the study had demonstrated impact and recommended further studies. Findings were also shared with national health authorities as they evaluate the potential inclusion of ivermectin in malaria control programmes.
Regina Rabinovich, BOHEMIA PI and Director of ISGlobal’s Malaria Elimination Initiative said: ‘This research has the potential to shape the future of malaria prevention, particularly in endemic areas where existing tools are failing. With its novel mechanism of action and proven safety profile, ivermectin could offer a new approach using a well-known, safe drug that can add to the effect of other mosquito control tools available today.’
The blood pressure lowering effect of nitrate-rich beetroot juice in older people may be due to specific changes in their oral microbiome, according to the largest study of its kind.
Researchers at the University of Exeter conducted the study, published in the journal Free Radical Biology and Medicine, comparing responses between a group of older adults to that of younger adults. Previous research has shown that a high nitrate diet can reduce blood pressure, which can help reduce risk of heart disease.
Nitrate is crucial to the body and is consumed as a natural part of a vegetable-rich diet. When the older adults drank a concentrated beetroot juice ‘shot’ twice a day for two weeks*, their blood pressure decreased – an effect not seen in the younger group.
The new study, funded by a BBSRC Industrial Partnership Award, provides evidence that this outcome was likely caused by the suppression of potentially harmful bacteria in the mouth. An imbalance between beneficial and harmful oral bacteria can decrease the conversion of nitrate (abundant in vegetable-rich diets) to nitric oxide. Nitric oxide is key to healthy functioning of the blood vessels, and therefore the regulation of blood pressure.
Study author Professor Anni Vanhatalo, of the University of Exeter, said: “We know that a nitrate-rich diet has health benefits, and older people produce less of their own nitric oxide as they age. They also tend to have higher blood pressure, which can be linked to cardiovascular complications like heart attack and stroke. Encouraging older adults to consume more nitrate-rich vegetables could have significant long term health benefits. The good news is that if you don’t like beetroot, there are many nitrate-rich alternatives like spinach, rocket, fennel, celery and kale.”
The study recruited 39 adults aged under 30, and 36 adults in their 60s and 70s through the NIHR Exeter Clinical Research Facility. The trial was supported by the Exeter Clinical Trials Unit. Each group spent two weeks taking regular doses of nitrate-rich beetroot juice and two weeks on a placebo version of the juice with nitrate stripped out. Each condition had a two week “wash out” period in between to reset. The team then used a bacterial gene sequencing method to analyse which bacteria were present in the mouth before and after each condition.
In both groups, the make-up of the oral microbiome changed significantly after drinking the nitrate-rich beetroot juice, but these changes differed between the younger and older age groups.
The older age group experienced a notable decrease in the mouth bacteria Prevotella after drinking the nitrate rich juice, and an increase in the growth of bacteria known to benefit health such as Neisseria. The older group had higher average blood pressure at the start of the study, which fell after taking the nitrate-rich beetroot juice, but not after taking the placebo supplement.
Co-author Professor Andy Jones, of the University of Exeter, said: “This study shows that nitrate-rich foods alter the oral microbiome in a way that could result in less inflammation, as well as a lowering of blood pressure in older people. This paves the way for larger studies to explore the influence of lifestyle factors and biological sex in how people respond to dietary nitrate supplementation.”
Dr Lee Beniston FRSB, Associate Director for Industry Partnerships and Collaborative Research and Development at BBSRC, said: “This research is a great example of how bioscience can help us better understand the complex links between diet, the microbiome and healthy ageing. By uncovering how dietary nitrate affects oral bacteria and blood pressure in older adults, the study opens up new opportunities for improving vascular health through nutrition. BBSRC is proud to have supported this innovative partnership between academic researchers and industry to advance knowledge with real-world benefits.”
Study analysed data from the US National Youth Tobacco Survey on more than 60 000 middle and high school students.
Photo by Nery Zarate on Unsplash
Adolescents who use either e-cigarettes or conventional tobacco products (CTP) – like cigarettes, cigars, hookah and pipes – are significantly more likely to report symptoms of depression and anxiety than teens who don’t use tobacco products at all, according to a study published this week in the open-access journal PLOS Mental Health by Noor Abdulhay of West Virginia University, USA, and colleagues.
Tobacco use and mental health challenges are known to have a complex, bidirectional relationship. Understanding the interplay between adolescent tobacco use and mental health is particularly important, since adolescence is a critical developmental period during which many health-related risk-taking behaviors begin. Moreover, there are increasing rates of anxiety, depression, and suicide among adolescents in the U.S. as well as shifting patterns of tobacco use.
In the new study, researchers used data on tobacco use, depression and anxiety symptoms, among different demographics, from the 2021-2023 National Youth Tobacco Survey. Among the 60,072 middle and high school students who had completed all questionnaires in full, 21.37% had used tobacco products, with 9.94% using only e-cigarettes, 3.61% using only CTPs, and 7.80% using both.
Overall, 25.21% of respondents reported symptoms associated with depression and 29.55% reported anxiety symptoms. Compared to adolescents who had not used any tobacco products, users of e-cigarettes or CTPs displayed a potentially heightened risk of depression and anxiety, whilst those who used both CTPs and e-cigarettes had the highest odds of reporting mental health struggles
The authors conclude that “while causality cannot be determined, the results from this study showed that all forms of tobacco use were significantly associated with mental health issues. There is a need to continue promoting mental health support and implementing tailored interventions to combat all forms of tobacco use among adolescents”.
