Category: 8. Health

CLINICAL CONVERSATIONS

Ketamine has made waves with its potential for treating major depressive disorder and mood disorders, but rarely do you hear of it being used to treat patients with eating disorders. New research from Denver’s Eating Recovery Center and Pathlight Mood & Anxiety Center highlights this important, underrecognized potential use of ketamine. With their new study, Elizabeth Wassenaar, MD, MS, DFAPA, CEDS-C, and her team have become the first in the world to demonstrate that ketamine can be administered safely in higher levels of care, even when patients are actively struggling with an eating disorder or malnutrition.¹

Psychiatric Times sat down with Wassenaar to better understand how ketamine can be used for patients with eating disorders, and how she and her team unlocked the potential of this treatment.

Psychiatric Times:Why this news is important for psychiatrists and mental health clinicians to see?

Elizabeth Wassenaar, MD, MS, DFAPA, CEDS-C: This is the first study of its kind to evaluate if ketamine can be used safely in a patient population with active eating disorders. Many psychiatrists and mental health clinicians may be fearful to treat individuals with eating disorders precisely because they do not know if it is safe for them to receive ketamine as a medication for their treatment-resistant depression. Psychiatrists and mental health professionals are familiar and may even be comfortable with prescribing ketamine for treatment-resistant depression but may have been hesitant to prescribe for individuals with eating disorders, with good reason.

Individuals with eating disorders often have medical complexities related to malnutrition that can increase their risk of respiratory depression with ketamine. Fortunately, we have been able to show that individuals with eating disorders, even those active in their disease and in varying degrees of malnutrition, with a body mass index down to 10, were able to receive subanesthetic generic intranasal ketamine without any medical incident or concerning change in vital signs. It is important for psychiatrists and mental health professionals to note that the patient population we studied were in a highly controlled and contained environment with significant support for both their psychological distress and their nutritional needs, and to use this information when planning for the care of their own patients.

PT: How can psychiatrists and mental health clinicians apply this in their own practice?

Wassenaar: Psychiatrists and mental health clinicians can apply this information as they work with individuals with eating disorders to consider if ketamine is an appropriate treatment option and to consider what kind of support their patients may need to assure safety from novel interventions.

PT: What does this new study reveal about using ketamine?

Wassenaar: This new study tells us that generic subanesthetic doses of intranasal ketamine can be used safely and a wide variety of patients with activating disorders at varying degrees of malnutrition when they are in a medically supervised environment.

PT: Why have patients with eating disorders been excluded from psychedelic research and treatment until now?

Wassenaar: Individuals with eating disorders are a difficult group of individuals to study precisely because of the medical instability that can be a consequence of the use of disordered eating behaviors. This can complicate and confound research questions and increase the demand for the psychological and medical needs of this population. In psychedelic research specifically, individuals are often required to be safe and stable at an outpatient level of care and weight restored, which for many individuals with eating disorders is a very high bar and may exclude them from important ongoing research on novel interventions for mental illness.

PT: Thank you!

Dr Wassenaar is the regional medical director for the Mountain and West regions at Eating Recovery Center and Pathlight Mood & Anxiety Center.

Reference

1. Wassenaar E, Blalock DV, Duffy A, et al. Is ketamine safe for individuals in higher level of care treatment for eating disorders? analysis of safety of subanesthetic ketamine in 104 patients. J Psychiatr Res. 2025:188:52-56.

Now, a study published on July 2 in Nature has uncovered compelling genomic evidence that points to air pollution—and other environmental exposures—as a potential major factor behind this growing public health concern. The study was jointly led by researchers at the University of California San Diego and the National Cancer Institute (NCI), part of the National Institutes of Health (NIH).

“We’re seeing this problematic trend that never-smokers are increasingly getting lung cancer, but we haven’t understood why,” said study co-senior author Ludmil Alexandrov, professor of bioengineering and cellular and molecular medicine at UC San Diego, and member of UC San Diego Moores Cancer Center. “Our research shows that air pollution is strongly associated with the same types of DNA mutations we typically associate with smoking.”

“This is an urgent and growing global problem that we are working to understand regarding never-smokers,” said Maria Teresa Landi, epidemiologist in the Division of Cancer Epidemiology and Genetics at the NCI and co-senior author of the study. “Most previous lung cancer studies have not separated data of smokers from non-smokers, which has limited insights into potential causes in those patients. We have designed a study to collect data from never-smokers around the world and use genomics to trace back what exposures might be causing these cancers.”

And while previous studies in the literature have shown an epidemiological link between air pollution and lung cancer in never-smokers, this new research goes further by showing a genomic link.

Mutational effects of air pollution

The team analyzed lung tumors from 871 never-smokers living in 28 regions with different levels of air pollution across Africa, Asia, Europe and North America. Using whole-genome sequencing, the researchers identified distinct patterns of DNA mutations—known as mutational signatures—that act like molecular fingerprints of past exposures.

By combining these genomic data with pollution estimates based on satellite and ground-level measurements of fine particulate matter, the researchers were able to estimate individuals’ long-term exposure to air pollution. They found that never-smokers living in more polluted environments had significantly more mutations in their lung tumors, particularly driver mutations—which directly promote cancer development—and mutational signatures linked to cancer—which serve as a record of all past mutagenic exposures. For example, these individuals had a 3.9-fold increase in a mutational signature linked to tobacco smoking and a 76% increase in another signature linked to aging.

This doesn’t mean that pollution causes a unique “air pollution mutational signature” per se, noted study co-first author Marcos Díaz-Gay, a former postdoctoral researcher in Alexandrov’s lab who is now a junior group leader at the Spanish National Cancer Research Center (CNIO) in Madrid, Spain. Rather, it increases the overall number of mutations, particularly in known pathways of DNA damage. “What we see is that air pollution is associated with an increase in somatic mutations, including those that fall under known mutational signatures attributed to tobacco smoking and aging,” said Díaz-Gay.

The researchers also noted a dose-response relationship: the more pollution someone was exposed to, the more mutations were found in their lung tumors. These tumors also had shorter telomeres—the protective caps on the ends of chromosomes—which is a sign of accelerated cellular aging.

Surprising finding from secondhand smoke exposure

In contrast, the researchers did not find a strong genetic correlation with secondhand smoke. Lung tumors of never-smokers exposed to secondhand smoke showed only a slight increase in mutations, along with shorter telomeres, but no distinct mutational signatures or driver mutations. While exposure to secondhand smoke is a known cancer risk, its mutational effect was far less pronounced than that seen with air pollution. “If there is a mutagenic effect of secondhand smoke, it may be too weak for our current tools to detect,” said study co-first author Tongwu Zhang, an Earl Stadtman Investigator in the Biostatistics Branch of the NCI. “However, its biological effects are still evident in the significant telomere shortening.”

The researchers acknowledged that their analysis could be further limited by the complexity of measuring secondhand smoke exposure. “It’s difficult to get that kind of information because it depends on various factors such as amount of time one was exposed; how far one was from exposure; and how often one shared a space with someone else who smoked, for example,” said Díaz-Gay.

Risk found from herbal medicine

In addition to air pollution, researchers identified another environmental risk: aristolochic acid, a carcinogen found in certain traditional Chinese herbal medicines. A specific mutational signature linked to aristolochic acid was found almost exclusively in lung cancer cases of never-smokers from Taiwan. Though aristolochic acid has previously been linked to bladder, gastrointestinal, kidney and liver cancers from ingestion, this is the first study to report evidence that it may contribute to lung cancer. The researchers suspect that these cases may arise from inhalation of traditional Chinese herbal medicines, but more data are needed to support their hypothesis.

“This raises new concerns about how traditional remedies might unintentionally raise cancer risk,” said Landi. “It also presents a public health opportunity for cancer prevention—particularly in Asia.”

New signature, new questions

In another intriguing discovery, the team identified a new mutational signature that appears in the lung cancers of most never-smokers but is absent in smokers. Its cause remains unknown—it did not correlate with air pollution or any other known environmental exposure. “We see it in a majority of cases in this study, but we don’t yet know what’s driving it,” said Alexandrov. “This is something entirely different, and it opens up a whole new area of investigation.”

Next steps

Moving forward, the researchers are expanding their study to include lung cancer cases of never-smokers from Latin America, the Middle East and more regions of Africa. The researchers are also turning their attention to other potential risks. One focus is on marijuana and e-cigarette use, particularly among younger people who have never smoked tobacco. The team is investigating whether these exposures may also contribute to mutational changes in lung tissue. They also aim to study other environmental risks—such as radon and asbestos—as well as gather more detailed pollution data at local and individual levels.

Full study: “The mutagenic forces shaping the genomes of lung cancer in never smokers.”

This work was supported by the Intramural Research Program of the National Cancer Institute, part of the National Institutes of Health (project ZIACP101231); NIH grants R01ES032547-01, R01CA269919-01, and 1U01CA290479-01; a Packard Fellowship for Science and Engineering; and UC San Diego Sanford Stem Cell Institute.

Disclosures: Ludmil B. Alexandrov is a co-founder, CSO, scientific advisory member and consultant for io9. Alexandrov has equity in and receives income from io9. The terms of this arrangement have been reviewed and approved by the University of California San Diego in accordance with its conflict of interest policies. Alexandrov is also a compensated member of the scientific advisory board of Inocras. Alexandrov’s spouse is an employee of Biotheranostics. Alexandrov and study co-author Erik N. Bergstrom declare a U.S. provisional patent application filed with UC San Diego with serial numbers 63/269,033. Alexandrov also declares U.S. provisional applications filed with UC San Diego with serial numbers: 63/366,392; 63/289,601; 63/483,237; 63/412,835; and 63/492,348. Alexandrov is also an inventor of a U.S. Patent 10,776,718 for source identification by non-negative matrix factorization. Alexandrov and study co-first author Marcos Díaz-Gay further declare a European patent application with application number EP25305077.7. Study co-author Soo-Ryum Yang has received consulting fees from AstraZeneca, Sanofi, Amgen, AbbVie and Sanofi; and received speaking fees from AstraZeneca, Medscape, PRIME Education and Medical Learning Institute. All other authors declare that they have no competing interests.

Air pollution has been linked to a swathe of lung cancer-driving DNA mutations, in a study of people diagnosed with the disease despite never having smoked tobacco.

The findings from an investigation into cancer patients around the world helps explain why never-smokers make up a rising proportion of people developing the cancer, a trend the researchers called an “urgent and growing global problem”.

Prof Ludmil Alexandrov, a senior author on the study at the University of California in San Diego, said researchers had observed the “problematic trend” but had not understood the cause. “Our research shows that air pollution is strongly associated with the same types of DNA mutations we typically associate with smoking,” he said.

The scientists analysed the entire genetic code of lung tumours removed from 871 never-smokers in Europe, North America, Africa and Asia as part of the Sherlock-Lung study. They found that the higher the levels of air pollution in a region, the more cancer-driving and cancer-promoting mutations were present in residents’ tumours.

Fine-particulate air pollution was particularly linked to mutations in the TP53 gene. These have previously been associated with tobacco smoking. People exposed to greater air pollution also had shorter telomeres, protective strands of DNA found at the ends of chromosomes, which are often compared with the caps on shoelaces. Telomeres tend to shorten with age, so premature telomere shortening is interpreted as a sign of rapid ageing.

“This is an urgent and growing global problem that we are working to understand,” said Dr Maria Teresa Landi, an epidemiologist on the study at the US National Cancer Institute in Maryland.

With smoking in decline in many parts of the world, including the UK and the US, never-smokers are making up a larger proportion of lung cancer patients. Current estimates suggest that 10-25% of lung cancers are now diagnosed in never-smokers. Almost all are a form of cancer known as adenocarcinoma.

Lung cancer remains the leading cause of cancer-related death worldwide. About 2.5m new cases are diagnosed globally each year. More than a million of the deaths occur in China, where smoking, air pollution and other environmental contaminants are factors.

Recent research found that the highest rates of adenocarcinoma attributable to air pollution were in east Asia. While cases in the UK were much lower, they still amounted to more than 1,100 new diagnoses a year, scientists found.

The latest work, published in Nature, identified only a slight rise in cancer-causing mutations in people exposed to secondhand tobacco smoke. But the study highlighted a significant risk from certain Chinese herbal medicines that contain aristolochic acid. Signature mutations linked to the herbal medicines were seen almost exclusively in never-smokers from Taiwan.

Another mysterious mutational signature was seen in never-smokers but not smokers. “This is something entirely different,” Alexandrov said.

PROVIDENCE, R.I. [Brown University] — Triclosan is an antimicrobial chemical that was for decades added to everyday items like soap, toothpaste, cosmetics and even kitchen utensils and athletic wear, until concerns about potential health risks led manufacturers to phase it out of some products.

New research suggests there may be even more reason for concern. 

A study led by scientists at Brown University and the University of Massachusetts Amherst found that children with higher levels of triclosan in their bodies were more likely to have allergy-related health issues, with young boys appearing most affected.      

Published in Environmental Health Perspectives, the study followed 347 mothers and their children from pregnancy through the kids’ 12th birthdays. As part of the Cincinnati-based Health Outcomes and Measures of the Environment Study, researchers analyzed urine samples collected up to 10 times over that period to assess triclosan exposure in children. 

They found that children with higher levels of the chemical were more likely to develop allergic conditions like eczema and hay fever, a common allergy that causes sneezing, congestion and itchy eyes.

“The research showed a clear connection between this chemical and the allergic conditions we looked at,” said study senior author Joseph Braun, a professor of epidemiology and director of the Center for Climate, Environment and Health at Brown University’s School of Public Health. “What that all means is antimicrobial chemical exposure during susceptible periods of life, childhood in this case, might increase the risk of allergic disease.” 

The study found that children with twice the level of triclosan in their urine were 23% more likely to report eczema symptoms. This risk increased to nearly 40% by the time they were 8 to 12 years old. Similarly, children with twice the level of triclosan were 12% more likely to have symptoms of hay fever. Boys whose mothers had higher levels of triclosan during pregnancy were more likely than girls to show allergy symptoms.

The same reasons that make triclosan a health concern are in part what made it popular, said Hannah Laue, lead author of the study and an assistant epidemiology professor at UMass Amherst.

“Triclosan is effective at killing many bacteria, fungi and viruses,” Laue said. “While that’s useful for extending product shelf life or reducing odors in athletic wear, it can be harmful to humans. Our bodies rely on beneficial microbes to aid digestion and protect against pathogens. Exposure to triclosan may disrupt that healthy balance, leaving us more vulnerable to disease.”

Laue added that triclosan can also interfere with hormonal systems. 

“Some chemicals, including triclosan, can mimic or block hormones, potentially throwing essential systems into overdrive or shutting them down,” she said. “Triclosan has also been linked to reduced thyroid hormone levels, which are critical for healthy growth and development.”

A persistent antimicrobial

The U.S. Food and Drug Administration banned triclosan from over-the-counter hand soaps in 2016. Since then, many companies have voluntarily removed it from toothpaste and other products. Yet the chemical is still found in some consumer goods, including antimicrobial cutting boards, personal care items and clothing. Manufacturers are not required to list triclosan on product labels. 

The new study is part of an effort by Braun’s team to understand how antimicrobial chemicals affect children’s health. Working with Laue and others, the group has focused on the health effects of triclosan for the last three years, and they plan to track the young study participants into adulthood. The researchers are especially interested in how triclosan might disrupt the gut microbiome, which helps regulate immune responses, and what that means for adolescent and long-term health outcomes.

Braun and Laue hope this body of research will encourage both consumers and manufacturers to make safer choices.

“People can reduce their triclosan exposure by doing what they can to avoid products that contain it,” Braun said. “We also hope that this will prompt companies to consider using safer antimicrobial chemicals or avoiding them altogether in their products.”

The study was supported by the National Institute of Environmental Health Sciences and the National Center for Advancing Translational Sciences. Additional Brown University authors included Elvira Fleury, who earned a master of public health from Brown in 2024 and is now a doctoral student at Harvard University. 

This transcript has been edited for clarity. 

Hello, everyone. I’m Dr Bishal Gyawali, associate professor of oncology at Queens University, Kingston, Canada. I’m very happy to share with you some of the most exciting data that I just saw at the plenary session at ASCO 2025. 

Before that, I’m going to talk to you about a fantastic new drug called exercisumab. I’m joking, of course. Exercise has been shown to improve the lives of patients with colon cancer. I’m joking that if there were a drug called exercisumab, the data would be so compelling that we’d all want to use it and fund it today. 

Because this is not a drug and it’s about exercise, I see some challenges in implementation. I hope that I’m able to convince you that the data are really compelling and we should make an effort so that our health systems will integrate this as a part of cancer care for patients with high-risk stage II and stage III colon cancer who receive adjuvant chemotherapy. 

The trial I’m talking about is called the CHALLENGE trial, which was not presented at the plenary but should have been. In this trial, patients who had high-risk stage II and stage III colon cancer, after they completed their adjuvant chemotherapy, were randomized to receive a structured exercise program vs the standard-of-care arm. 

The standard-of-care arm patients received health education but did not receive a structured exercise program. The goal of the structured exercise program was to improve physical activity by at least 10 MET-hours compared to the baseline of these patients. 

The primary endpoint was disease-free survival. Disease-free survival was significantly improved, and overall survival was also significantly improved. The 5-year disease-free survival rates improved by almost 7%, and the 8-year overall survival rates also improved by a similar amount. The hazard ratio for disease-free survival was 0.72, and the hazard ratio for overall survival was 0.63. 

These are very compelling results. If you compare these results with results from other trials, you’ll see that this is a no-brainer. If this were a drug, you would want to use it today. 

There are some nuances about this trial that I want to highlight. When we talk about the results, some of the comments were, “Oh yes, I have been asking my patients to exercise anyway.” Exercise improves quality of life, it’ll reduce weight, and these are all known to benefit patients. 

I have been telling my patients to exercise, but this trial is not about telling patients to exercise. This trial is about having a formal, structured exercise program. There are particular details.

Patients need to have an in-person visit with a therapist every 2 weeks for the first year and then every month for the next 2 years, so it’s a 3-year therapy program. It’s a scientifically designed and tailored program. It’s not just saying, oh, you should exercise. In fact, saying you should exercise and giving some health education was the control arm of this treatment, not the interventional arm.

The control arm patients were told about this trial, the potential benefits of the exercise, why they should enroll in this trial, and they were given health education materials. An interesting observation is that even the control arm patients had improvements in their physical functioning, VO₂, and all those parameters from baseline to subsequent visits. 

One limitation is the adherence rate to exercise. We see that the adherence rate kept falling with time. I think that by the end of 3 years, the adherence rate to the exercise program was around 60%-65% in that ballpark, which is a limitation. Having said that, the analysis accounts for all of that.

Despite that limitation, we are seeing this substantial benefit. If you want to compare that with the ATOMIC trial, which was a plenary presentation of immunotherapy plus FOLFOX for patients who needed adjuvant FOLFOX in stage III colon cancer patients, of course, the addition of atezolizumab to FOLFOX improved disease-free survival rates. The primary endpoint here was 3-year disease-free survival, and it improved significantly. It was a plenary, and people were making the argument that this should immediately change practice. 

If you compare that with this exercise trial that I just discussed: A, think about the added toxicities; B, think about the added cost; and C, think about how feasible it is to implement. I think it’s a no-brainer that we need to start having health systems funds for a structured exercise program for our patients with colon cancer. 

Yes, the atezolizumab data and the ATOMIC trial data look very interesting and this is one of the first advances in treatment of adjuvant colon cancer in a long time. This is for patients with microsatellite instability-high status. We don’t have overall survival results yet. Disease-free survival is a much more reliable predictor of overall survival in this particular setting. I believe that overall survival might be positive, but we also need to know what percentage of these patients got immunotherapy when they relapsed, because immunotherapy is already standard of care for these patients when they relapse. 

The other point about this trial is, do they all actually need 1 year of atezolizumab? Probably not. As the discussant highlighted in her talk, in many settings, we are now using neoadjuvant strategies. Using two or three cycles might be enough.

The broader point that I’m trying to make is contrasting these two studies and inviting you to think about how different these are, even in terms of magnitude of benefit. The exercise trial has overall survival, not just disease-free survival, at an 8-year time point. 

When I asked Dr Booth about the cost of this intervention, he said for the whole 3-year time point, it might be around $3000 Canadian dollars. This trial was conducted mostly in Canada and in Australia. As opposed to atezolizumab, where a month of atezolizumab alone is going to cost $15,000, so that’s just a perspective I wanted to put forward. 

One more thing I wanted to talk about today is the SERENA-6 trial, which was discussed at the plenary session. This is a trial for patients with estrogen receptor-positive, HER2-negative metastatic breast cancer who have been on a CDK4/6 inhibitor plus aromatase inhibitor for 6 months. They were then tested with ctDNA to detect ESR1 mutations early, and if this was detected, then they were randomized to either follow the same treatment, which is the control arm, or get the new drug.

The primary endpoint here was progression-free survival. This was debated often during the season. We have so many debates about progression-free and overall survival, but for this particular trial, progression-free survival makes no sense because this is just detecting relapse early. Detecting relapse early does not always mean that you need to intervene early.

Of course, if you are intervening early, then you are going to prolong time to tumor progression. The progression-free survival in this sense is more like time on treatment with this drug rather than true progression-free survival. You’re just changing treatment early, and the control arm patients are not getting that treatment when they progress.

Measuring progression-free survival alone here felt similar to measuring CA-125, or whatever tumor markers we measure, then instituting treatment early and claiming that patients have a longer time on treatment, when in fact, it’s just lead time bias or intervening early without knowing that it’s going to improve outcomes.

A final trial from the plenary session was the MATTERHORN trial. I want to bring that up as well because this trial was investigating durvalumab plus perioperative FLOT in patients with esophageal cancers. This trial had a significant improvement in event-free survival, but has not improved overall survival yet. It may or may not translate into an overall survival improvement. 

The discussant did not cover the limitations of this trial well, and that’s why I wanted to bring it up. There are several factors to consider here. There are other trials in similar settings, where event-free or disease-free survival have improved, but overall survival has not. There is no point in getting super excited about this because it may not translate to overall survival, just like other immunotherapy trials in this space. 

The other thing is, we need to make sure what treatments patients are getting at the time of progression or at the time of relapse. Are they getting the right treatment?If they’re not getting the right treatment, then any survival difference can be simply a function of the control arm patients not getting the right treatment at the time of relapse. 

If we compare these results with results of other immunotherapy trials, I don’t think the results are substantially different. Yes, an event-free survival improvement is important, but especially in this setting, in this disease, we have seen other trials where disease-free or event-free survival have not necessarily led to an overall survival improvement. We need to be asking ourselves, can we claim that it is already practice changing without having those results? I don’t think that’s the case. 

Those are some of my thoughts from this year’s plenary session at ASCO 2025. Thank you.

Investigators have found that two common types of hormone therapy may alter breast cancer risk in women before age 55. Women treated with unopposed estrogen hormone therapy (E-HT) were less likely to develop the disease than those who did not use this type of hormone therapy. Additionally, women treated with estrogen plus progestin hormone therapy (EP-HT) were more likely to develop breast cancer than women who did not use this type of hormone therapy. Together, these results—published by O’Brien et al in The Lancet Oncology—may help to guide clinical recommendations for hormone therapy use among younger women.

The two hormone therapies analyzed in the study are often used to manage symptoms related to menopause or following hysterectomy or oophorectomy. Unopposed estrogen therapy is recommended only for women who have had a hysterectomy because of its known association with uterine cancer risk.

“Hormone therapy can greatly improve the quality of life for women experiencing severe menopausal symptoms or those who have had surgeries that affect their hormone levels,” said lead author Katie O’Brien, PhD, of the National Institutes of Health’s (NIH) National Institute of Environmental Health Sciences (NIEHS). “Our study provides greater understanding of the risks associated with different types of hormone therapy, which we hope will help patients and their doctors develop more informed treatment plans.”

Key Results

The researchers conducted a large-scale analysis that included data from more than 459,000 women younger than age 55 across North America, Europe, Asia, and Australia. Women who used E-HT had a 14% reduction in breast cancer incidence compared with those who never used this type of hormone therapy. Of note, this protective effect was more pronounced in women who started E-HT at younger ages or who used it longer. In contrast, women using EP-HT experienced a 10% higher rate of breast cancer compared with nonusers, with an 18% higher rate seen among women using EP-HT for more than 2 years relative to those who never used this type of therapy.

According to the authors, this suggests that for EP-HT users, the cumulative risk of breast cancer before age 55 could be about 4.5%, compared with a 4.1% risk for women who never used this type of hormone therapy and a 3.6% risk for those who used E-HT. Further, the association between EP-HT and breast cancer was particularly elevated among women who had not undergone hysterectomy or oophorectomy. That highlights the importance of considering gynecologic surgery status when evaluating the risks of starting hormone therapy, the researchers noted.

“These findings underscore the need for personalized medical advice when considering hormone therapy,” said NIEHS scientist and senior author Dale Sandler, PhD. “Women and their health-care providers should weigh the benefits of symptom relief against the potential risks associated with hormone therapy, especially EP-HT. For women with an intact uterus and ovaries, the increased risk of breast cancer with EP-HT should prompt careful deliberation.”

The authors noted that their study is consistent with previous large studies that documented similar associations between hormone therapy and breast cancer risk among older and postmenopausal women. This new study extends those findings to younger women, providing essential evidence to help guide decision-making for women as they go through menopause.

Disclosure: For full disclosures of the study authors, visit thelancet.com.

Uterine cancer is the fourth most common cancer diagnosed in women in the United States, with about 69,120 new cases and nearly 14,000 deaths from the disease expected this year. Black women experience a twice as high mortality rate compared with women of other races and ethnicities, and that number is expected to rise sharply over the coming decades.

According to a study by Wright et al published in Cancer Epidemiology, Biomarkers & Prevention, the incidence and mortality rates of uterine cancer in the United States are projected to increase significantly over the next 3 decades, with incidence-based mortality expected to be nearly three times higher in Black women compared with White women.

Study Methodology

The researchers developed the Columbia University Uterine Cancer Model (CU-UTMO) as part of the National Cancer Institute’s Cancer Intervention and Surveillance Modeling Network (CISNET). This state-transition microsimulation model simulates the trajectories for uterine cancer incidence and mortality based on characteristics from a sample population, taking into account age (between 18 and 84 years); Black and White race; birth cohort grouped in 10-year intervals starting in 1910 to 1920; cancer stage, as determined by the American Joint Committee on Cancer; and separately modeled endometrioid and nonendometrioid tumors, which usually have a worse prognosis.

To validate the model, the researchers used CU-UTMO to predict the median age of diagnosis, survival rate, and distribution of diagnosis by stage for uterine cancer in 2018; they found those projections were comparable to the actual Surveillance, Epidemiology, and End Results data from that year. Then the researchers estimated the future rates of the cancer based on publicly available sources through 2018.

Key Results

The researchers found that the model closely fit population-based incidence and mortality data of uterine cancer. They determined that from 2020 to 2050, the incidence of uterine cancer is projected to increase in White women to 74.2 cases per 100,000 (compared with 57.7 cases per 100,000 in 2018) and to increase to 86.9 cases per 100,000 (compared with 56.8 cases per 100,000 in 2018) in Black women.

Among White women, incidence-based mortality will increase from 6.1 per 100,000 in 2018 to 11.2 per 100,000 in 2050, and incidence-based mortality in Black women will increase from 14.1 per 100,000 to 27.9 per 100,000. In addition, the incidence of endometrioid tumors is expected to increase considerably in both White and Black women. However, although White women will experience only a slight increase in nonendometrioid tumors, the incidence of these tumors in Black women will increase substantially.

“These population-level trends support the urgent need to develop and implement novel primary and secondary prevention strategies for uterine cancer,” concluded the study authors.

Understanding Disease Disparities

“There are likely a number of factors that are associated with the increased burden of uterine cancer in Black women,” said lead study author Jason D. Wright, MD, the Sol Goldman Professor of Gynecologic Oncology at Columbia University Vegelos College of Physicians and Surgeons. “They more commonly have aggressive types of uterine cancer, face delayed diagnosis resulting in later-stage disease at diagnosis, and there are often delays in their treatment.”

Reducing Burden of Disease

In addition to building this state-transition microsimulation model of uterine cancer, Dr. Wright and his colleagues also performed a stress test of the model by incorporating hypothetical screening and intervention methods that could detect uterine cancer and precancerous changes prior to a clinical diagnosis. They found that the screening and intervention methods were most effective when introduced at age 55, with declines in cancer incidence that lasted up to 15 years in White women and up to 16 years in Black women.

“The stress testing suggests that if there was an effective screening test, we may be able to substantially reduce the burden of disease. While there is presently no screening or prevention that is routinely used for uterine cancer, we are currently examining the potential impact of integrating screening for this cancer into practice,” said Dr. Wright.

Disclosure: Funding for this study was provided by the National Cancer Institute. For full disclosures of the study authors, visit aacrjournals.org/cebp.

Let’s be honest—deciding to raise your child vegan can feel like a deeply meaningful and intentional choice. You’ve done the research. You’ve had the debates (some louder than others). You’ve stocked your pantry with lentils, B12 supplements, and maybe a few “cheese” options that taste more like regret than dairy replacement.

But here’s what most people don’t tell you.

Raising vegan kids isn’t just about nutrition or ethics—it’s also about navigating tricky social dynamics, your own doubts, and other people’s projections. A lot of projections.

So if you’re considering this path—or already deep into it—here are seven things I wish someone had warned me about from the start.

1. You’ll second-guess yourself more than you expected

Even if you’re confident in your decision, there will be moments that shake you.

A birthday party where your kid stares longingly at a cupcake. A pediatrician visit that ends in side-eyes. A relative who says, “But don’t children need meat to grow?”

And suddenly, you find yourself lying awake at 2 a.m. Googling “Do vegan kids get enough protein?” even though you’ve read 12 articles confirming they do.

This doesn’t mean you’re doing anything wrong. It means you’re a thoughtful parent. But the self-doubt can be exhausting.

Here’s what helped me: grounding in facts (like the American Dietetic Association’s position that well-planned vegan diets are appropriate for all life stages), connecting with other plant-based families, and reminding myself that every parent questions themselves—whether their kid eats chicken nuggets or chickpea nuggets.

2. Other parents might treat you like you’re judging them

I can’t count how many times I’ve said, “We’re raising them vegan, but we really don’t expect other people to do the same,” only to be met with defensiveness.

You’d be amazed at how quickly “Oh, we don’t eat animal products” turns into “So you think I’m a bad mom?”

This is the psychological phenomenon of moral discomfort at work. As noted by Dr. Melanie Joy, author of Why We Love Dogs, Eat Pigs, and Wear Cows, “When people perceive a challenge to their beliefs, even if indirect, they often experience defensiveness—even if no one’s actually judging them.”

I’ve learned to lead with curiosity, not conviction. If someone asks why our family is vegan, I’ll share—but I don’t try to convert. That helps defuse tension and keeps the focus where it should be: on the kids’ well-being.

3. School lunchrooms can be emotional minefields

Let’s talk about the moment your kid opens their lunchbox at school and hears, “Ew, what’s that?”

It’s not just about being different—it’s about being visibly different during one of the most socially sensitive parts of the day. And kids can be brutally honest.

My son once came home asking if I could pack him something “normal,” like Lunchables. Not because he wanted meat—but because he didn’t want to be the odd one out.

This is where resilience-building comes in.

We started role-playing responses. Practicing how to explain his food choices without sounding defensive. Making lunches that look fun and familiar (thank you, cookie cutter sandwiches and cute fruit skewers).

Helping your child feel proud of who they are—and what they eat—is part of the job description.

4. You’ll get surprisingly emotional about “firsts”

First steps. First words. First ice cream cone.

But when you’re raising a vegan kid, these moments take on extra layers.

I cried the first time we found a fully vegan cupcake at a bakery. Not because it tasted amazing (it did), but because I didn’t have to say “no.” For once, my kid could just be a kid.

You’ll also feel an odd sense of grief when they miss out on certain traditions—like roasting marshmallows at camp or decorating eggs at Easter. It’s not about the food. It’s about the memories.

But here’s the upside: you’ll get creative. We toast vegan marshmallows over tealight candles. We dye wooden eggs. You find ways to make new traditions that feel just as magical.

5. Doctors and dietitians are hit or miss

Some will cheer you on. Others will raise an eyebrow and ask if your child is iron-deficient—even if their labs are fine.

I once had a pediatrician suggest “just adding a little fish” to my daughter’s diet because “kids need DHA.” Never mind that she was already getting DHA from algal oil supplements.

This is where it pays to be politely assertive. Bring data. Ask questions. Be open, but also trust yourself.

As registered dietitian Reed Mangels has said, “A vegan diet can meet nutrient needs during pregnancy, infancy, and childhood when properly planned.”

If a healthcare provider doesn’t support that—or makes you feel shamed for your choices—it’s okay to find a new one. Seriously.

6. Your kid will ask questions you’re not always ready for

“Why don’t we eat what my friends eat?”
“Does the cow get sad?”
“Will Grandpa stop eating animals someday, too?”

Whew.

These are not yes-or-no questions. They’re big, philosophical inquiries wrapped in little voices. And they deserve thoughtful answers.

But they also hit you when you least expect them—like in the car line at school or while brushing teeth.

I’ve learned not to overcomplicate it. I keep explanations honest, age-appropriate, and rooted in our family values.

And when I don’t know how to answer, I say so. Then we figure it out together.

7. It’s not just about food—it’s about identity

One of the most unexpected things I’ve realized is how deeply food ties into a child’s sense of self.

When your child says, “I’m vegan,” they’re not just describing a dietary choice—they’re claiming a value system. One that might make them feel different from their peers.

And that’s both beautiful and complicated.

I’ve seen my daughter explain to her classmates that we don’t go to the zoo because we care about animals’ freedom. I’ve watched her ask if her soccer shoes are made from leather. She’s 8.

That kind of awareness can be powerful—but it can also feel heavy.

So we make space to talk about it. To explore what it means to live with integrity and openness. To stand up for your beliefs without putting others down.

That’s the long game, isn’t it? Not just raising vegan kids—but raising thoughtful, kind, critically-thinking humans.

Final thoughts

No one has all the answers. There will be slip-ups. Questions you didn’t prepare for. Snacks eaten at a friend’s house you didn’t approve of.

And that’s okay.

Raising vegan kids isn’t about perfection—it’s about intention. It’s about showing up, staying curious, and leading with values that matter to you.

If you’re navigating this path too, just know: you’re not alone. And you’re doing better than you think.

Turkey said on Wednesday it will shut down all livestock marketplaces to control the spread of highly contagious foot and mouth disease, reported Reuters. 

The agriculture ministry said it detected a new serotype of the disease that heightened the outbreak, due to animal movement after the Muslim religious holiday of Eid al Adha, which is typically marked by slaughtering livestock.

The decision was taken to prevent further spread as teams continue to vaccinate animals against the disease, the ministry said. It will gradually lift the restrictions once the entirelivestock population is vaccinated.

The ministry also said the temporary closure will not disrupt supply and demand for meat and dairy products in Turkey.

Introduction

Sarcopenia is a progressive disorder characterized by the loss of muscle mass and strength. And it is particularly prevalent among older adults, it might affect up to half of people aged 80 years and older, posing a significant public health challenge. In older adults with type 2 diabetes mellitus (T2DM), the prevalence of sarcopenia is 2–3 times higher than in non-diabetic peers.¹ This dual burden not only impairs physical performance and quality of life but also increases the risk of falls, frailty, and mortality.² In recent years, growing concerns have arisen regarding the potential impact of glucose-lowering medications on muscle health, generating significant clinical debate. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are commonly used hypoglycemic agents. They work through several mechanisms, including increasing glucose-dependent insulin secretion, inhibiting glucagon secretion during hyperglycemia, delaying gastric emptying, and reducing caloric intake. Semaglutide, a long-acting GLP-1RA, can be administered subcutaneously once weekly. It effectively lowers glucose levels and promotes significant weight loss, making it widely adopted for the treatment of diabetes and obesity.^3,4 Additionally, it has shown therapeutic effects on sarcopenic obesity.⁵ However, concerns have been raised about the potential for muscle loss due to long-term Semaglutide use. Some studies indicate that elevated GLP-1 levels may have a detrimental effect on muscle mass.⁶ Given that elderly patients are at a higher risk for sarcopenia, it is essential to further investigate how Semaglutide treatment affects skeletal muscle in this population. In this study, we examined changes in muscle mass and strength among elderly type 2 diabetes patients using Semaglutide, aiming to provide evidence-based guidance for its clinical application.

Methods

Study Design and Participants

This retrospective cohort study investigated older patients (≥65 years) with T2DM who initiated Semaglutide therapy at our hospital between January 2022 and December 2022. Propensity score matching (1:1 ratio) was performed based on age, sex, baseline BMI, diabetes duration, and comorbidities. The resulting control group had comparable baseline characteristics but was not exposed to GLP-1RAs or DPP-4 inhibitors. All participants were monitored for 24 months, with data collected at baseline (0 months), 6 months, 12 months, 18 months, and 24 months. Inclusion criteria were as follows: Age ≥65 years with T2DM (according to ADA guidelines), Body mass index (BMI) ≥24kg/m², with no prior use of GLP-1RA or DPP-4 inhibitors. The study had certain criteria that excluded individuals who had severe liver or renal impairment (defined as serum alanine transaminase (ALT) ≥ 3-fold the upper limit of normal; estimated glomerular filtration rate (eGFR)<15mL/ min/1.73 m²) and cancer. Study subjects meeting the eligibility criteria were included after comprehensive validation of data completeness via the electronic health records system, with exclusion of any cases lacking essential variables. All participants received individualized glucose-lowering regimens supervised by endocrinology specialists. Semaglutide dosage was adjusted based on both glycemic monitoring and hemoglobin A1c levels. This study was approved by the Ethics Committee of Shijiazhuang People’s Hospital (Approval No: 2025075) and conducted by the Declaration of Helsinki. All participants provided written informed consent prior to data collection. Patient confidentiality was protected by anonymizing all personal identifiers in the dataset. The reporting followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines.

Data Collection

Demographic and clinical parameters were systematically extracted from electronic medical records. This data included age, sex, BMI, muscle parameters, duration of diabetes, and comorbidities. The chronic diseases considered included cerebrovascular disease, coronary heart disease, kidney disease, hypertension, and chronic obstructive pulmonary disease (COPD). Due to the retrospective study design, standardized assessments of lifestyle factors (dietary intake and physical activity) were unavailable in the source dataset.

Muscle parameters were assessed through measurements of muscle mass and function. Skeletal muscle mass was estimated using bioelectrical impedance analysis (BCA-1C, Tongfang Health Technology, Beijing). Upper extremity muscle strength was evaluated through handgrip strength measurements, taken with an electronic hand dynamometer (CAMRY EH101, Guangdong). Lower limb muscle strength was evaluated using a 4-meter gait speed test, calculated as gait speed (m/s) = 4 (m) ÷ time (s).

The appendicular skeletal muscle mass index (ASMI) was calculated by dividing the appendicular lean mass of the arms and legs by the square of height (kg/m²). Sarcopenia diagnosis followed 2019 Asian Working Group for Sarcopenia (AWGS) criteria,⁷ requiring both low muscle mass (ASMI <7.0 kg/m² males, <5.7 kg/m² females) and reduced muscle strength (handgrip strength <28 kg males, <18 kg females).

Statistical Analysis

Data were statistically analyzed using IBM SPSS 27.0 and GraphPad 9.0. Continuous variables with normal distribution were expressed as mean ± standard deviation (Mean ± SD). Between-group comparisons used independent samples t-tests, while intra-group longitudinal changes were analyzed with paired t-tests. Categorical variables were compared via chi-square tests. Multivariable linear regression models were constructed to identify clinical predictors of accelerated muscle loss during Semaglutide treatment, adjusting for potential confounders. A two-tailed p-value <0.05 defined statistical significance.

Results

The analysis included 220 Semaglutide-treated patients and 212 matched controls. The baseline information of the Semaglutide treatment group is shown in Table 1. Sarcopenia prevalence was 27.73% in the study population. No significant differences were observed in baseline characteristics between the two groups. However, at the 24-month follow-up, the Semaglutide-treated group exhibited significantly lower values for BMI, ASMI, handgrip strength, and gait speed compared to the control group (p< 0.05). Detailed results are presented in Table 2.

Table 1 Baseline Characteristics of Semaglutide-Treated Patients

Table 2 Comparison of Anthropometric and Muscle Parameters Between Semaglutide-Treated and Control Patients

Longitudinal Changes in Anthropometric and Muscle Parameters

Weight and Muscle Mass Dynamics

All subjects treated with Semaglutide showed a continuous reduction in BMI throughout the study period (p<0.001). A non-significant downward trend in ASMI emerged at 6 months, with significant reductions observed from month 12 onward. Cumulative ASMI loss reached 0.39 kg/m² in females and 0.26 kg/m² in males by study end. While the control group also showed sustained ASMI decline, the magnitude was markedly smaller than in the treatment group (Figure 1).

Figure 1 Longitudinal changes in BMI and muscle parameters during the study period. (a) BMI trajectories. (b) AMSI changes. (c) Handgrip strength variations. (d) Gait speed dynamics. Compare of Semaglutide group: male #<0.05, ##<0.01, ###<0.001; female #<0.05, ##<0.01, ###<0.001. Compare of control group: male *<0.05, **<0.01, ***<0.001; female *<0.05, **<0.01, ***<0.001.

Muscle Strength Trajectories

Handgrip strength: Males displayed a transient improvement at 6 months, followed by a progressive decline. Female participants, while showing no statistically significant change at 6 months, exhibited an upward trend that was subsequently followed by significant deterioration. Gait speed: Both genders exhibited similar patterns, with non-significant declines in intermediate phases but statistically significant overall reductions. Refer to Figure 2 for more information. Semaglutide-treated patients showed significantly greater reductions in ASMI, handgrip strength and gait speed compared to controls (see Table 2).

Figure 2 Multivariable regression analysis of predictors for muscle mass loss following semaglutide treatment. Semaglutide dosage, ASMI, and Gait speed were significant influences. Muscle mass loss (kg/m2) =1.536 + 0.096 × Semaglutide dosage ‒ 0.076 × ASMI + 0.004 × Hand grip strength ‒ 0.892 × Gait speed (R2=0.337).

Influential Factors of Semaglutide-Associated Muscle Loss

To identify determinants of muscle loss, we performed correlation analysis followed by multiple linear regression. The initial correlation analysis revealed that gender, age, baseline body mass index, diabetes duration, and chronic comorbidities showed no significant association with muscle mass loss. However, significant correlations were found with Semaglutide dosage, baseline ASMI, handgrip strength, and gait speed. As shown in Table 3.

Table 3 Correlation Analysis of the Variables with Muscle Loss

Subsequent multiple linear regression analysis, using muscle mass loss as the dependent variable and Semaglutide dosage, baseline ASMI, handgrip strength, and gait speed as independent variables, confirmed independent associations for semaglutide dosage, baseline ASMI, and gait speed, whereas handgrip strength lost statistical significance. The regression model (R² = 0.337) predicted muscle mass loss as: Muscle mass loss (kg/m²) =1.536+0.096×Semaglutide dosage-0.076× ASMI+0.004×Hand grip strength-0.892×Gait speed, R²=0.337. As displayed in Figure 2.

Discussion

Sarcopenia is an age-related condition characterized by the progressive loss of skeletal muscle mass and strength. It typically begins after the age of 30, at a rate of 0.1% to 0.5% annually, and accelerates beyond the age of 65 due to physiological and metabolic changes in aging populations.⁸ In this study, we investigated the effects of Semaglutide on muscle health in elderly patients with T2DM. Our analysis reveals that while Semaglutide effectively reduces body weight in elderly T2DM patients, it paradoxically accelerates this physiological muscle decline, particularly at higher doses and in individuals with pre-existing low muscle mass and function.

The weight-loss effects of Semaglutide, a long-acting GLP-1RA, are well-established,⁹ and this was confirmed in our elderly cohort. This weight loss may be linked to its ability to suppress appetite, delay gastric emptying, and regulate satiety signaling in the central nervous system.¹⁰ In older patients with T2DM, weight loss not only improves glycemic control but also reduces the risk of cardiovascular disease,¹¹ which is especially important in this population. However, despite the metabolic benefits of weight loss, it is crucial to consider the components of that weight loss. Our study found that weight loss was accompanied by a reduction in muscle mass and a decline in muscle function, which could negatively affect the long-term health of elderly patients. This finding contrasts with results from previous studies,¹² possibly because our follow-up population consisted entirely of elderly individuals. Skeletal muscle is the largest organ system in adults, accounting for approximately 30–45% of body weight in young adults, and it plays a vital role in protein homeostasis, as it contains the largest amount of body protein. Maintaining protein homeostasis, or net protein balance, is essential for muscle health. Under certain conditions, such as prolonged fasting, starvation, or inadequate protein intake, skeletal muscle can break down its proteins to mobilize amino acids.¹³ Semaglutide reduces body weight by suppressing appetite and decreasing energy intake; this diminished protein intake may lead to the body breaking down muscle proteins to provide necessary amino acids.¹⁰ Thus, using Semaglutide in older patients with T2DM may exacerbate the development of sarcopenia due to negative energy balance. Moreover, high doses of Semaglutide may more robustly suppress appetite and energy intake,¹⁴ leading to exacerbated muscle mass loss. The precise molecular mechanisms underlying this phenomenon require further investigation. These findings prompt critical inquiry into whether targeted protein supplementation may attenuate these effects in older populations – a promising avenue for future investigation.

Interestingly, we observed that Semaglutide initially improved muscle function, although in female participants this improvement only manifested as an upward trend. This effect may be mediated through the reduction of intramuscular fat infiltration, which is characteristically elevated in obese individuals. The accumulation of lipids and their metabolic byproducts within and between muscle cells can lead to mitochondrial dysfunction and subsequent declines in muscle strength and function.¹⁵ Previous studies have confirmed that GLP-1RA treatment significantly reduces this pathological fat infiltration.¹⁶ However, our data demonstrate that long-term administration results in gradual muscle mass loss, ultimately attenuating the initial functional improvements.

Our regression analysis identified baseline ASMI and gait speed as independent predictors of muscle loss, without significant gender or age differences. This suggests that reduced physical activity, resulting from declining muscle function, may create a vicious cycle of further muscle deterioration.¹⁷ Current research has shown that physical activity, particularly resistance training, has therapeutic effects on sarcopenia.¹⁸ Whether muscle loss can be prevented in Semaglutide users by increasing exercise participation needs further investigation.

The findings of this study have significant implications for clinical practice. While Semaglutide has notable benefits in improving glycemic control and promoting weight loss, its adverse effects on muscle mass should not be overlooked, especially in elderly patients. Clinicians should consider the following points when prescribing Semaglutide: (1) Patient selection: Carefully evaluate the risks and benefits of Semaglutide in elderly patients or those with pre-existing sarcopenia. (2) Dose adjustment: Start elderly patients on a low dose and gradually adjust according to their tolerance and response, avoiding high doses. (3) Monitoring and intervention: Regularly monitor muscle mass, physical function, and quality of life during Semaglutide treatment. This could be combined with moderate resistance training and optimized protein intake,¹⁹ if needed, to help slow muscle loss.

This study has several limitations. The relatively small sample size may limit the generalizability of the findings. While we accounted for major known confounders, we were unable to assess nutritional intake and physical activity patterns, which could influence muscle outcomes. Additionally, the observational nature of the study prevents causal conclusions. These limitations highlight the need for future prospective studies with standardized assessments of diet and exercise.

Conclusion

The use of Semaglutide is associated with muscle loss and functional decline in older adults with type 2 diabetes, particularly at higher doses. This effect is especially significant in patients with sarcopenia. Consequently, it is crucial to assess the risks and benefits for each elderly patient individually and to implement appropriate monitoring and interventions. The potential for nutritional supplementation and targeted exercise regimens to counteract semaglutide-associated muscle decline merits systematic investigation.

Data Sharing Statement

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

Ethics Approval and Consent to Participate

The study was approved by the Ethics Committee of Shijiazhuang People’s Hospital (Approval No: 2025075). All methods were performed by the Declaration of Helsinki, and the reporting followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines.

Acknowledgments

We are grateful to all the patients who accepted to participate in this study.

Funding

There is no funding to report.

Disclosure

The authors declare that they have no competing interests in this work.

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