Empagliflozin was associated with a 22 per cent lower risk of progression from early stages of diabetic retinopathy to more advanced stages in this patient group.
Diabetic retinopathy (DR) affects about 26 per cent of people with diabetes. While many patients have an early form of DR, the condition can progress, posing the threat of irreversible vision loss. Empagliflozin is a sodium-glucose contratransporter-2 inhibitor (SGLT-2), an oral medication that helps patients with type 2 diabetes control their glucose levels. A research team led by investigators from Mass General Brigham conducted a cohort study comparing treatment with empagliflozin to another form of diabetes treatment for patients with type 2 diabetes. They found that while empagliflozin did not reduce the risk of DR in patients with no history of that disease, among patients who had early-stage DR, the medication was associated with a decreased risk of progression.
“Our findings showed that in patients with type 2 diabetes and non-proliferative diabetic retinopathy, empagliflozin could be beneficial in slowing down progression to more advanced stages of diabetic retinopathy,” said lead author Helen Tesfaye, PharmD, MSc, of the Division of Pharmacoepidemiology at Brigham and Women’s Hospital. “Our findings could help inform clinical decision-making for patients with diabetes who have non-proliferative diabetic retinopathy or are at risk for developing DR.”
The study represents a collaboration between Brigham and Women’s Hospital (BWH) and Massachusetts General Hospital (MGH), both founding members of the Mass General Brigham healthcare system, with experts from BWH’s Division of Renal (Kidney) Medicine and MGH’s Diabetes Center working with Tesfaye and colleagues from the Division of Pharmacoepidemiology.
“Leveraging the clinical and analytical expertise of our multidisciplinary team allows us to identify risks and benefits of diabetes medications that are not being studied—or may not be apparent—in clinical trials,” said Deborah Wexler.
Involving local leaders and churches is integral in addressing chronic health problems.
With Type 2 diabetes on the rise, prevention measures are critical. However, it’s often hard for people living in rural areas to access health care and lifestyle resources that can improve their health.
According to a recent study from the University of Georgia, involving local leaders and churches could make all the difference in these communities.
Working with the UGA Archway Partnership, researchers and community members implemented the Centers for Disease Control and Prevention’s Diabetes Prevention Program across rural Georgia.
The program is designed to help people develop healthy habits that can prevent the onset of Type 2 diabetes. However, the program has limited reach in rural areas.
“In having conversations with our community partners, we realized that there might be an opportunity to address diabetes in rural areas,” said Henry Young, co-author of the study and a professor at UGA’s College of Pharmacy. “The community was very involved, engaged and excited to participate.”
This initiative could pave the way for more programs focused on improving health in underserved communities.
Social connection helps cement lifestyle changes.
The CDC program consists of modules centred around topics such as increasing physical activity. The course is spread over a year, with the first half dedicated to establishing healthy habits while the second focuses on maintaining them.
During these sessions, participants discussed what was going well for them and any challenges they faced, and tips were provided that helped them make healthier choices. They also provided much-needed support to one another.
“They created and shared recipes,” said Young. “They went on walks together. Social engagement and interpersonal interactions helped address overall health and well-being.”
With the small size of many rural communities, the researchers found that bonds with other members may be key in encouraging lifestyle changes. In turn, these initiatives can strengthen existing community bonds.
Adopting healthier habits takes local support.
Getting people to change their behaviours can be challenging. Participants sticking to traditional diets and a slow-paced lifestyle seen in many rural areas may lead to resistance to change and a tendency for people to be set in their ways regarding diet and exercise.
So, the researchers worked with local churches and community leaders to encourage adopting these new healthy habits.
Twenty churches were involved in the program, with 33 life coaches from the local community trained to help facilitate discussions during each one-hour session. Most of those lifestyle coaches came from the churches.
The researchers then conducted interviews with these coaches and religious leaders to understand how participants felt about their health and the program.
“The participants always went above one hour because they were so engaged in the discussion,” said Smita Rawal, lead author of the study and a postdoctoral associate from UGA’s College of Pharmacy. “People were so open to discussing their health as well as helping each other and motivating each other to adopt healthier lifestyles.”
Rural regions face unique barriers to accessing healthcare
Participants cited transportation as a significant obstacle to participating in community events.
Many of them also struggled with different health issues, which made attending sessions more challenging.
To overcome these challenges, community members, including churches and their leadership, arranged for vans or organized carpooling to make meetings more accessible for those without reliable transportation. And some lifestyle coaches also made home visits for those who missed sessions due to illness.
“To be successful, we need to identify and address barriers,” said Young. “But then we also need to leverage resources to support these healthier lifestyle interventions.”
The active components of these elements of the Mediterranean diet show promise in treating atherosclerosis and reducing the risk of heart attacks and strokes.
Cardiovascular problems are the leading cause of disease and mortality worldwide. Plant extracts, rich in bioactive compounds, have contributed significantly to the development of drugs, as they offer therapeutic potential for several of these diseases. However, their use is limited by possible side effects, drug-drug interactions and the lack of scientific evidence from quality preclinical and clinical studies.
During the 2023/24 academic year, biologist Mateu Anguera Tejedor made an essential contribution in this field with his final year Biology degree project at the UAB, tutored by the then postdoctoral researcher at the Institut de Neurociències of the UAB (INc-UAB) and current lecturer at the Faculty of Pharmacy and Food Sciences of the University of Barcelona, René Delgado.
The study, recently published as a scientific article in the journal Food Bioscience, provides an overview of the mechanisms of action and the preclinical and clinical evidence, as well as the adverse effects of essential bioactive compounds derived from a group of selected Mediterranean plants which form part of the Mediterranean diet.
Among the species analysed, six representative plants and their major active components are reported: garlic (Allium sativum, with diallyl trisulfide, allicin and S-allyl [cysteine]), hawthorn shrub (Crataegus monogyna, with quercetin, apigenin and chlorogenic acid), saffron (Crocus sativus, with crocin and safranal), olive (Olea europaea, with oleic acid, oleuropein, hydroxytyrosol and oleacein), rosemary (Salvia rosmarinus, with rosmarinic acid and carnosic acid) and grapevine (Vitis vinifera, with resveratrol). The review focused on the most critical pharmacological mechanisms, including their antioxidant, anti-inflammatory and vasodilatory actions, and their regulation of lipid metabolism, which may be relevant for conditions such as atherosclerosis and hypertension. The results show that these active components are promising in potentially treating atherosclerosis and could reduce the risk of heart attacks and strokes.
In addition to summarising the current scientific evidence, the study provides a reference guide for future research by identifying potential knowledge gaps and offering timely recommendations for designing preclinical and clinical studies in this area. Key areas for future exploration include the long-term safety of these compounds, the evaluation of their synergistic effects when consumed as part of a Mediterranean diet, and the need to establish standardised protocols in controlled clinical settings. By broadening the scientific basis of these traditional remedies, this review may help pave the way for their use as active pharmaceutical ingredients in developing future phytomedicines.
Combined ingestion could alter the efficacy of individual extracts.
The research team believes that using these natural extracts is promising. Still, their combined ingestion could influence therapeutic outcomes due to the “matrix effect”, which implies that dietary components can alter the efficacy of each extract, either enhancing or diminishing their benefits. Understanding this interaction is essential to optimise the therapeutic application of these plant extracts in a dietary context. It is vital to recognise that there is often a lack of robust evidence of the impact of natural extracts in humans, and therefore, researchers caution that “the label of ‘natural’ does not guarantee safety, and this emphasises the need to prioritise pharmacokinetic, toxicological and clinical studies to evaluate their efficacy, safety and efficiency in comparison with existing drugs”.
Graphical abstract of the work. Credit Mount Sinai Health System
Diabetes researchers and bioinformaticians from the Icahn School of Medicine at Mount Sinai have developed a new understanding of how human beta cell regenerative drugs work. These drugs, developed at Mount Sinai, may hold promise for more than 500 million people with diabetes worldwide.
Diabetes develops when cells in the pancreas, known as beta cells, cannot produce insulin, a hormone essential to regulating blood sugar levels. While significant progress has been made toward discovering a durable therapy, none are scalable therapeutic options for millions of diabetics worldwide.
For more than 15 years, researchers at the Icahn School of Medicine at Mount Sinai have worked tirelessly to find a solution to cure diabetes by identifying a drug that could make human beta cells regenerate.
In 2015, Mount Sinai researchers discovered the first such drug, called harmine. Harmine is a member of a class of medications called DYRK1A inhibitors. In 2019 and 2020, the researchers reported that DYRK1A inhibitors could synergize with TGF-beta signalling as well as GLP-1 receptor agonist (GLP-1RA) drugs such as semaglutide (e.g., Ozempic) and exenatide (Byetta) to induce more robust levels of human beta cell regeneration. Finally, in July 2024, they showed that harmine alone increases human beta cell mass by 300 per cent, and if a GLP-1RA is added, by 700 per cent.
A key question has been how harmine causes beta cells to regenerate. In the newest study, the research team reports that the new, regenerated beta cells may be coming from an unexpected source: a second pancreatic cell type called alpha cells. Since alpha cells are abundant in people with type 1 and type 2 diabetes, they may be able to serve as a source for new beta cells in both common types of diabetes.
“This is an exciting finding that shows harmine-family drugs may be able to induce lineage conversion in human pancreatic islets,” says Esra Karakose, PhD, Assistant Professor of Medicine (Endocrinology, Diabetes and Bone Disease) at the Icahn School of Medicine at Mount Sinai and corresponding author of the study. “It may mean that people with all forms of diabetes have a large potential ‘reservoir’ for future beta cells, just waiting to be activated by drugs like harmine.”
“A simple pill, perhaps together with a GLP1RA like semaglutide, is affordable and scalable to the millions of people with diabetes,” said Dr. Stewart.
The interplay of genes + environment alters key aspects of brain structure at a young age, boosting susceptibility.
Reducing early exposure to parental smoking may decrease the risk of developing multiple sclerosis (MS) in individuals who are genetically predisposed to the disease, according to research published in the Journal of Neurology, Neurosurgery & Psychiatry.
Research indicates that the interaction between genetic factors and environmental influences, such as smoking, changes essential aspects of brain structure during early childhood. This alteration may contribute to the development of the disease, suggesting there might be a critical window of opportunity to prevent it.
Multiple sclerosis (MS) is an autoimmune disease typically diagnosed between the ages of 20 and 40. Researchers explain that it is unclear whether it results from early inflammatory brain damage or a latent neurodegenerative process accompanied by inflammation.
While the exact onset of the disease process remains unclear, evidence of brain volume loss and diminished cognitive performance before the appearance of clinical signs and symptoms indicates that these changes may occur before a formal diagnosis.
Studies on migration show that early life environmental factors have a key role, but they add that exactly how these interact isn’t yet known.
The researchers used data from the population-based Dutch Generation R study to shed more light on how and when the interplay of environmental and genetic risk factors might affect brain volume and, thus, facilitate future MS development.
Participants in this study had good-quality data on genotype and/or the known environmental risk factors of Epstein Barr virus infection, vitamin D levels, weight (BMI), parental tobacco exposure, and outdoor activity at the age of 5, plus high-quality brain scan images at the ages of 9 and 13.
In all, the researchers drew on imaging data showing brain volume for 5350 participants and brain microstructure for 5649 participants, none of whom had been diagnosed with MS.
Polygenic risk scores derived from DNA samples were used to assess the genetic risk of developing MS, with the genetic variant rs10191329 used as a marker of future MS severity.
In all, 642 children tested positive for Epstein-Barr virus infection, and 405 had been exposed to household parental smoking.
The final analysis was based on genetic data from 2817 participants and brain volume and microstructure imaging data from 2970 participants.
This showed an interplay between genetic and environmental risk factors for MS associated with certain aspects of brain structure during childhood and early teens.
Specifically, higher genetic risk for MS was associated with a strong immune response to Epstein-Barr virus infection, and it was also associated with increased susceptibility to the negative effects of household parental smoking on brain development.
Higher MS genetic risk and household parental smoking interacted and were associated with lower total brain volume and grey matter volume, including thalamic volume.
No associations were observed for carriers of the rs10191229 genetic valiant.
This is an observational study, so no firm conclusions about cause and effect can be drawn.
The researchers explain the findings by pointing out that higher Epstein-Barr virus antibodies may be caused by defective immune system control of this virus due to genetic risk for MS, possibly facilitating the development of the disease later in life.
And the prevailing theory is that tobacco smoke produces chronic inflammation of the respiratory tract, thereby increasing the inflammatory activity of the immune system, they add.
“Our results importantly add another potential mechanism of tobacco smoke exposure in individuals with higher polygenic MS risk. The increased brain vulnerability to the effects of parental smoking may increase the exposure of [central nervous system] antigens to the developing immune system, increasing the risk of a brain-specific autoimmune disease,” they suggest.
“How this increased vulnerability influences other MS risk factors may open a window for prevention of MS by limiting childhood exposure to household smoking or other toxic exposures associated with MS (i.e., household chemicals), and should be a focus for further studies” they conclude.
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