Category: 8. Health

Intermittent energy restriction, time-restricted eating and continuous energy restriction can all improve blood sugar levels and body weight in people with obesity and type 2 diabetes, according to a study being presented Sunday at ENDO 2025, the Endocrine Society’s annual meeting in San Francisco, Calif.

“This study is the first to compare the effects of three different dietary interventions intermittent energy restriction (IER), time-restricted eating (TRE) and continuous energy restriction (CER) in managing type 2 diabetes with obesity,” said Haohao Zhang, Ph.D., chief physician at The First Affiliated Hospital of Zhengzhou University in Zhengzhou, China.

Although researchers identified improved HbA1c levels, and adverse events were similar across the three groups, the IER group showed greater advantages in reducing fasting blood glucose, improving insulin sensitivity, lowering triglycerides, and strengthening adherence to the dietary interventions.

“The research fills a gap in directly comparing 5:2 intermittent energy restriction with a 10-hour time-restricted eating in patients with obesity and type 2 diabetes. The findings provide scientific evidence for clinicians to choose appropriate dietary strategies when treating such patients,” Zhang said.

Zhang and colleagues performed a single-center, randomized, parallel-controlled trial at the First Affiliated Hospital of Zhengzhou University from November 19, 2021 to November 7, 2024.

Ninety patients were randomly assigned in a 1:1:1 ratio to the IER, TRE or CER group, with consistent weekly caloric intake across all groups. A team of nutritionists supervised the 16-week intervention.

Of those enrolled, 63 completed the study. There were 18 females and 45 males, with an average age of 36.8 years, a mean diabetes duration of 1.5 years, a baseline BMI of 31.7 kg/m², and an HbA1c of 7.42%. 

At the end of the study, there were no significant differences in HbA1c reduction and weight loss between the IER, TRE and CER groups. However, the absolute decrease in HbA1c and body weight was greatest in the IER group. 

Compared to TRE and CER, IER significantly reduced fasting blood glucose and triglycerides and increased the Matsuda index, a measure of whole-body insulin sensitivity. Uric acid and liver enzyme levels exhibited no statistically significant changes from baseline in any study group.

Two patients in the IER group and the TRE group, and three patients in the CER group, experienced mild hypoglycemia. 

The IER group had the highest adherence rate (85%), followed by the CER group at 84% and the TRE group at 78%. Both the IER and CER groups showed statistically significant differences compared with the TRE group.

Zhang said these findings highlight the feasibility and effectiveness of dietary interventions for people who have obesity and type 2 diabetes.

About Endocrine Society
Endocrinologists are at the core of solving the most pressing health problems of our time, from diabetes and obesity to infertility, bone health, and hormone-related cancers. The Endocrine Society is the world’s oldest and largest organization of scientists devoted to hormone research and physicians who care for people with hormone-related conditions.

The Society has more than 18,000 members, including scientists, physicians, educators, nurses, and students in 122 countries. To learn more about the Society and the field of endocrinology, visit our site at www.endocrine.org. Follow us on X (formerly Twitter) at @TheEndoSociety and @EndoMedia.

We know that a complex combination of factors contribute to Alzheimer’s disease risk, including genetics, mental health, and diet. New research suggests that breast cancer survival could be part of the overall picture too.

The new research, led by a team from institutions across South Korea, found that there was an 8 percent lower risk of Alzheimer’s in women who have survived breast cancer, based on an average follow-up of 7.3 years.

That may well be down to the effects of radiation therapy, according to the researchers. The findings run counter to some previous studies that have linked cancer treatments to a decline in cognitive abilities – so-called ‘chemobrain’.

Related: A Signal of Future Alzheimer’s Could Be Hidden in The Way You Speak

“A substantial number of breast cancer survivors report cancer-related cognitive impairment, experiencing difficulties in concentration and memory during and after cancer treatment,” write the researchers in their paper.

“However, evidence regarding the risk of Alzheimer dementia among breast cancer survivors remains mixed and inconclusive and may vary by age at diagnosis, treatment received, and time since treatment.”

The new study is based on health records of 70,701 patients who had been diagnosed with breast cancer and given treatment for it, compared to 180,360 healthy controls. Across the study period, Alzheimer’s incidence was 8 percent lower in the cancer group.

It’s not a huge difference: for every 1,000 women followed for a year, the statistics would predict Alzheimer’s would develop in 2.45 breast cancer survivors, compared to 2.63 women who hadn’t had cancer. The data can’t prove direct cause and effect either, because of the observational nature of the research.

Nevertheless, that altered risk level may add up over time and across larger groups, especially when other factors are added in. The clearest statistical significance for the risk reduction was in the over-65s, due to there being more cases of Alzheimer’s in older people.

The stats showed the risk reduction was greatest for those given radiation treatment for cancer, and that the risk reduction disappeared over time. That suggests this type of treatment may have effects we don’t fully understand, although radiation therapy has previously been associated with reducing inflammation in the brain.

“The risk of Alzheimer’s dementia is a crucial aspect of overall well-being among breast cancer survivors,” write the researchers.

“Concerns about chemobrain and the long-term adverse effects of breast cancer treatment on cognition are common, but our findings suggest that this treatment does not directly lead to Alzheimer’s dementia.”

Breast cancer survival rates continue to improve. If it’s detected early, more than nine out of 10 women can expect to survive. However, it also remains the most common cancer in women in most countries.

This latest research adds some useful extra context to the health issues and complications that might result from breast cancer and its associated treatments, especially in later life – and to ways we might ultimately be able to prevent Alzheimer’s from developing.

“Breast cancer survivors may have a slightly lower risk of Alzheimer’s dementia compared with cancer-free individuals, potentially influenced by cancer treatments, underscoring the need for further research on long-term neurocognitive outcomes in this population,” write the researchers.

The research has been published in JAMA Network Open.

Anti-obesity medications can significantly raise testosterone levels and improve health outcomes for men with obesity or type 2 diabetes, according to a new study being presented Monday at ENDO 2025, the Endocrine Society’s annual meeting in San Francisco, Calif.

Testosterone not only plays a critical role in the body when it comes to male sexual functioning, but it can also have an impact on an individual’s bone mass, fat distribution, muscle mass, strength and red blood cell production. Increases in body weight and prevalence of type 2 diabetes are often associated with lowered testosterone levels, resulting in fatigue, decreased libido and quality of life.

“While it is well known that weight loss from lifestyle changes or bariatric surgery increases testosterone levels, the impact that anti-obesity medications may also have on these levels has not been widely studied,” said Shellsea Portillo Canales, M.D., endocrinology fellow at SSM Health St. Louis University Hospital in St. Louis, Mo. “Our study is among the first to provide compelling evidence that low testosterone can be reversed with the use of commonly prescribed anti-obesity medications.”

To test this hypothesis, researchers analyzed the electronic health records of 110 adult men with obesity or type 2 diabetes being treated with the weight-loss medications semaglutide, dulaglutide or tirzepatide and who were not on testosterone or hormonal therapy. Participants’ total and free testosterone levels were measured before and during treatment over the course of 18 months. 

Along with 10% weight loss, the proportion of men with normal levels of both total and free testosterone rose from 53% to 77%. These findings indicate that anti-obesity medications also can have a positive effect on the reproductive health of men with obesity or type 2 diabetes.

“Results from this study show that there is a direct correlation between the use of anti-obesity medications and testosterone levels,” said Portillo Canales. “Doctors and their patients can now consider this class of medications not only for the treatment of obesity and to control blood sugar, but also to benefit men’s reproductive health.”

About Endocrine Society
Endocrinologists are at the core of solving the most pressing health problems of our time, from diabetes and obesity to infertility, bone health, and hormone-related cancers. The Endocrine Society is the world’s oldest and largest organization of scientists devoted to hormone research and physicians who care for people with hormone-related conditions.

The Society has more than 18,000 members, including scientists, physicians, educators, nurses, and students in 122 countries. To learn more about the Society and the field of endocrinology, visit our site at www.endocrine.org. Follow us on X (formerly Twitter) at @TheEndoSociety and @EndoMedia.

Popular anti-obesity medications continue to be effective for weight loss even when availability and access is interrupted, according to a study being presented by a private weight-loss company Monday at ENDO 2025, the Endocrine Society’s annual meeting in San Francisco, Calif. 

“Patients taking GLP-1 treatments like semaglutide and tirzepatide often face challenges consistently accessing their medications due to supply shortages or insurance coverage obstacles,” said Kaelen L. Medeiros, M.S., director of data and research at privately held weight-loss company Calibrate in New York, N.Y. “While unpredictable GLP-1 medication access is frustrating, the good news is that our research shows effective weight loss can still be achieved if paired with appropriate lifestyle changes and coaching support.”

Researchers looked at how interruptions to GLP-1 medication access impacted weight-loss outcomes in real-world patients taking part in a commercial metabolic health program that also included intensive lifestyle intervention. Participants followed an intensive lifestyle change curriculum that emphasized the four pillars of metabolic health: food, exercise, sleep and emotional health, while receiving one-on-one health coaching.

The study reviewed records for 6,392 participants who had at least one month of GLP-1 access and completed at least one year in an obesity and overweight care program. Of these participants, 72.5% experienced at least one disruption in their GLP-1 treatment and 11.1% had multiple disruptions. Participants received an average of 8.13 GLP-1 fills during the first year of research and 15.25 fills during the second year.

After 12 months, participants who faced access issues achieved 13.7% weight loss in 12 months and 14.9% in 24 months. Those without treatment interruptions had 17% weight loss in 12 months and 20.1% in 24 months. Those who received only 1 to 4 treatments over 12 months also achieved clinically significant weight loss, with more than 10% change in body weight on average.

“Given the often-unpredictable availability and shifting insurance coverage associated with anti-obesity medications, it’s important that patients understand the significant impact that lifestyle changes and coaching paired with treatment can have on their health outcomes,” Medeiros said.

While findings indicate that significant weight loss is still possible for those with inconsistent access to GLP-1 medications, Medeiros said the results found that a consistent medication course combined with lifestyle changes and support remains the most effective weight-loss program option. 

About Endocrine Society
Endocrinologists are at the core of solving the most pressing health problems of our time, from diabetes and obesity to infertility, bone health, and hormone-related cancers. The Endocrine Society is the world’s oldest and largest organization of scientists devoted to hormone research and physicians who care for people with hormone-related conditions.

The Society has more than 18,000 members, including scientists, physicians, educators, nurses, and students in 122 countries. To learn more about the Society and the field of endocrinology, visit our site at www.endocrine.org. Follow us on X (formerly Twitter) at @TheEndoSociety and @EndoMedia.

Florida Atlantic University researchers have secured two key grants to investigate targeting a gene for the first time as a new approach to treat glioblastoma, a very aggressive and fast-growing type of brain cancer.

Malignant gliomas, such as glioblastoma multiforme and astrocytomas, are the most common type of primary brain tumor in the United States. They make up about 78% of all malignant brain tumors. Although these tumors are not very common, especially in the U.S., they cause a high number of cancer deaths because they are so aggressive.

These awards, granted by the Florida Department of Health’s Cancer Connect program for $562,000 and the Palm Health Foundation for $50,000, support a distinctive collaboration among FAU researchers that unites complementary expertise in neuroscience and cancer biology. Together, this partnership aims to advance highly innovative projects that have the potential to make a meaningful impact on cancer therapy.

The grants will explore a promising new target – a gene called MBLAC1 – whose properties encouraged a collaboration between two FAU research labs, one focused on molecular neuroscience and the other on cancer mechanisms and treatment.

MBLAC1 plays a key role in regulating copper levels within cells, which affects mitochondrial function and oxidative stress – both critical factors in cancer cell survival and growth. Since glioblastoma cells rely heavily on mitochondrial energy production and protection against oxidative damage, targeting MBLAC1 could disrupt these processes and slow tumor progression.

Investigators of this grant are Randy D. Blakely, Ph.D., executive director of the FAU Stiles-Nicholson Brain Institute, the David J.S. Nicholson Distinguished Professor in Neuroscience and a professor of biomedical science within FAU’s Charles E. Schmidt College of Medicine; and Gregg B. Fields, Ph.D., FAU vice president for research and executive director of the FAU Institute for Human Health and Disease Intervention (I-Health).

By combining our expertise in cancer biology and neuroscience, we are approaching glioblastoma with a fresh and powerful perspective. By identifying how MBLAC1 supports tumor growth and testing drugs that block its function, our team hopes to lay the groundwork for developing new, effective therapies that could improve outcomes for patients with glioblastoma and possibly other cancers.”

Gregg B. Fields, Ph.D., FAU vice president for research and executive director of the FAU Institute for Human Health and Disease Intervention 

The project will investigate how MBLAC1 influences glioblastoma invasion and copper homeostasis using advanced 3D tumor models and genetically engineered mice lacking the gene.

“I’m excited to bring my background in neuroscience to explore new frontiers in cancer research,” said Blakely. “Our work centers on how a specific gene regulates copper – a vital micronutrient – in brain cells, which directly influences how these cells generate energy and manage stress. Because cancer cells depend heavily on energy to grow and spread, uncovering and interrupting this process could transform treatment. This collaboration is a perfect example of how combining different scientific perspectives can spark innovation and accelerate progress in the fight against cancer.”

The Blakely lab discovered that MBLAC1, a previously unstudied gene, plays a crucial role in brain cell function by regulating copper, which is essential for cell energy production and protection against oxidative stress. Lower levels of MBLAC1 have been linked to better survival in patients, suggesting it could be a key target for new treatments.

Researchers will investigate whether MBLAC1 from support brain cells or from the cancer cells themselves drives tumor invasion. Using 3D tumor models that closely mimic real tumors, they will observe how blocking MBLAC1 or copper affects tumor growth and spread. They are also developing a new test to quickly identify drugs that specifically inhibit MBLAC1 activity.

Blakely is collaborating on this project with cancer biologists Fields and Ania Knapinska, Ph.D., principal investigator and a research professor at FAU I-Health.

“Our project breaks new ground by uncovering a molecular pathway that actively promotes cancer through a gene linked to copper balance and glioblastoma risk,” said Knapinska. “We’re also pioneering novel genetic models to study glioblastoma in ways never done before. Our discoveries that mutations in this gene reduce mitochondrial function and increase cellular stress have driven us to explore its fundamental role in copper regulation and metabolism in living systems. Because this gene is highly targetable by drugs, our research opens promising new avenues for developing effective glioblastoma treatments.”

Glycogen is typically thought of as a reserve energy source stored in the liver and muscles. While small amounts also exist in the brain, particularly in support cells called astrocytes, its role in neurons has long been dismissed as negligible. “This new study challenges that view, and it does so with striking implications,” says Professor Pankaj Kapahi, PhD, senior scientist on the study. “Stored glycogen doesn’t just sit there in the brain; it is involved in pathology.”

The research team, led by postdoc Sudipta Bar, PhD, discovered that in both fly and human models of tauopathy (a group of neurodegenerative diseases including Alzheimer’s), neurons accumulate excessive glycogen. More importantly, this buildup appears to contribute to disease progression. Bar says tau, the infamous protein that clumps into tangles in Alzheimer’s patients, appears to physically bind to glycogen, trapping it and preventing its breakdown.

When glycogen can’t be broken down, the neurons lose an essential mechanism for managing oxidative stress, a key feature in aging and neurodegeneration. By restoring the activity of an enzyme called glycogen phosphorylase (GlyP) — which kicks off the process of glycogen breakdown — the researchers found they could reduce tau-related damage in fruit flies and human stem cell-derived neurons.

Rather than using glycogen as a fuel for energy production, these enzyme-supported neurons rerouted the sugar molecules into the pentose phosphate pathway (PPP) — a critical route for generating NADPH (nicotinamide adenine dinucleotide phosphate) and Glutathione, molecules that protect against oxidative stress. “By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies,” said Bar.

Even more promising, the team demonstrated that dietary restriction (DR) — a well-known intervention to extend lifespan — naturally enhanced GlyP activity and improved tau-related outcomes in flies. They further mimicked these effects pharmacologically using a molecule called 8-Br-cAMP, showing that the benefits of DR might be reproduced through drug-based activation of this sugar-clearing system. “This work could explain why GLP-1 drugs, now widely used for weight loss, show promise against dementia, potentially by mimicking dietary restriction,” said Kapahi.

Researchers also confirmed similar glycogen accumulation and protective effects of GlyP in human neurons derived from patients with frontotemporal dementia (FTD), strengthening the potential for translational therapies. Kapahi says the study emphasizes the power of the fly as a model system in uncovering how metabolic dysregulation impacts neurodegeneration. “Work in this simple animal allowed us to move into human neurons in a much more targeted way,” he said.

Kapahi also acknowledges the Buck’s highly collaborative atmosphere as a major factor in the work. His lab, with expertise in fly aging and neurodegeneration, took advantage of proteomics expertise in the Schilling lab and the Seyfried lab (at Emory University) as well as the Ellerby lab which has expertise in human iPSCs and neurodegeneration.

Kapahi says this study not only highlights glycogen metabolism as an unexpected hero in the brain but also opens up a new direction in the search for treatments against Alzheimer’s and related diseases. “By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell’s inner chemistry to fight age-related decline,” he says. “As we continue to age as a society, findings like these offer hope that better understanding — and perhaps rebalancing — our brain’s hidden sugar code could unlock powerful tools for combating dementia.”

Coauthors: Additional Buck collaborators include Kenneth A. Wilson, Tyler A.U. Hilsabeck, Sydney Alderfer, Jordan B Burton, Samah Shah, Anja Holtz, Enrique M. Carrera, Jennifer N. Beck, Jackson H Chen, Grant Kauwe, Tara E. Tracy, Birgit Schilling, and Lisa M. Ellerby. Other collaborators include Eric B. Dammer, Fatemeh Seifar and Nicholas T. Seyfried, Emory Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA as well as Ananth Shantaraman, Department of Biochemistry, Emory University School of Medicine, Atlanta, GA

Acknowledgments: The work was supported by NIH grants R01AG038688, R21AG054121, AG045835, R01AG071995, R01AG070193, T32AG000266-23, R01AG061879, P01AG066591 and 1S10 OD016281. Other support came from the Hevolution Foundation, American Federation of Aging Research, the Larry L. Hillblom Foundation and the Catalyst^X award from Alex and Bob Griswold

New research from the University of Pittsburgh School of Medicine and La Jolla Institute for Immunology, published today in Nature Microbiology, reveals an opportunity for developing a therapy against cytomegalovirus (CMV), the leading infectious cause of birth defects in the United States.

Researchers discovered a previously unappreciated mechanism by which CMV, a herpes virus that infects the majority of the world’s adult population, enters cells that line the blood vessels and contributes to vascular disease. In addition to using molecular machinery that is shared by all herpes viruses, CMV employs another molecular “key” that allows the virus to sneak through a side door and evade the body’s natural immune defenses.

The finding might explain why efforts to develop prophylactic treatments against CMV have, so far, been unsuccessful. This research also highlights a new potential avenue for the development of future antiviral drugs and suggests that other viruses of the herpes family, such as Epstein-Barr and chickenpox, could use similar molecular structures to spread from one infected cell to the next while avoiding immune detection.

If we don’t know what weapons the enemy is using, it is hard to protect against it. We found a missing puzzle piece that represents one possible reason why immunization efforts against CMV have been unsuccessful.”

Jeremy Kamil, Ph.D., senior author, associate professor of microbiology and molecular genetics at Pitt

In the United States, approximately one in every 200 babies is born with congenital CMV infection. Of the babies infected, one in five will have birth defects, such as hearing loss, or go on to have long-term health challenges. For most adults, CMV infections are asymptomatic. But a CMV infection during pregnancy presents significant health risks to the unborn child and could be deadly for people who are immunosuppressed, including organ transplant recipients.

Because of the large size of its genome and its complicated molecular machinery, CMV long evaded attempts to develop prophylactic treatments. Similar to other herpes viruses, CMV relies on a protein called gH to enter cells of the vessel lining. But unlike other herpes viruses, which use a protein partner called gL to facilitate infection, the new study found that CMV replaces gL with another partner called UL116 and recruits a protein called UL141. The resulting complex of gH-UL116-UL141, called GATE by the authors, then becomes an alternative tool for breaking into cells lining the blood vessels and causing internal damage while simultaneously preventing the body’s own immune system from recognizing the signs of infection.

The newly discovered GATE could become a potential vaccine target for CMV and other herpes viruses.

“Previous attempts to generate a CMV vaccine have failed, but that was before we identified the GATE complex. We hope that new strategies targeting GATE will improve our chances to combat CMV infection, and also perhaps cleanse our bodies of this lifelong infection,” said Chris Benedict, Ph.D., associate professor at La Jolla Institute for Immunology and co-senior author of the study with Kamil and LJI professor, president & CEO Erica Ollmann Saphire, Ph.D., MBA. “If we can develop antiviral drugs or vaccines that inhibit CMV entry, this will allow us to combat the many diseases this virus causes in developing babies and immune-compromised people.”

Other authors of this research are Michael Norris, Ph.D., of the University of Toronto; Lauren Henderson, Mohammed Siddiquey, Ph.D., both of Louisiana State University Health Shreveport; and Jieyun Yin, Ph.D., Kwangsun Yoo, Ph.D., Simon Brunel, Ph.D., Michael Mor, Ph.D., and Erica Ollmann Saphire, Ph.D., all of La Jolla Institute for Immunology.

This research was supported by the National Institutes of Health (grants AI11685, AI139749, AI101423 and T32HL155022) and by ARPA-H APECx contract 1AY1AX000055.