Whether it’s ABC Listen’s Health Report or Mamamia’s But Are You Happy, podcasts have quickly become part of our everyday media consumption. The average person spends more than five hours a week listening to them. But could listening to podcasts lead to healthier habits?
In a groundbreaking study, researchers at the University of South Australia have discovered that podcasts can significantly enhance health knowledge, increase exercise frequency, and promote healthier eating habits.
After reviewing the results of 38 studies, researchers found that people’s engagement with health-related podcasts was generally high. This suggests that podcasts could serve as an effective medium for delivering health information and promoting behaviour change interventions.
Nielsen data indicates that podcast popularity has risen by 16% since last year, solidifying this on-demand media in the daily lives of 9.6 million Australians.
UniSA researcher Beth Robins says the findings highlight the potential of podcasts promoting positive health behaviours.
“Health and wellbeing podcasts have the unique ability to convey a wide range of health topics to a variety of listeners, but in a very accessible way,” Robins says.
“Not only are podcasts typically chatty and conversational – which makes them easy to listen to and understand – but they’re also available at the touch of a button, so they’re extremely convenient, portable, and can be listened to at any time of the day.”
The study found that the most common motivations for listening to a health podcast was to gain information, better understand mental health issues, and to seek entertainment.
UniSA researcher Dr Ben Singh says the high engagement with health podcasts presents an advantage over other health interventions for sharing important public health messages.
“Our study is the first to review the evidence about health podcasts for the general population,” Dr Singh says.
“From this study, we know that podcasts are highly valued for their authenticity and reliability and their impactful, experience-focussed, and narrative-driven content.
“They’re also valued for their ability to be consumed at the user’s pace and in a setting that suits them – whether that’s while relaxing at home or walking the dog – and this aligns with increasing consumer demand for health resources that are both informative and adaptable to individual lifestyles.
“While more research is warranted, podcasts are clearly a highly engaging, well-received resource that can positively impact health behaviours and outcomes. It’s certainly a watch this space.”
PhD student Inbar Fischer Credit Tel Aviv University
A groundbreaking study from Tel Aviv University enhances our understanding of the biological mechanisms behind genetically based autism. It mainly focuses on mutations in the SHANK3 gene, which are responsible for nearly one million autism cases worldwide. Based on these findings, the research team applied a genetic treatment that improved the functioning of cells affected by the mutation, paving the way for future therapies for SHANK3-related autism.
The study was led by the lab of Prof. Boaz Barak and PhD student Inbar Fischer from the Sagol School of Neuroscience and the School of Psychological Sciences at Tel Aviv University.
Prof. Barak: “Autism is a common neurodevelopmental disorder affecting 1-2% of the global population, with one in every 36 boys in the U.S. diagnosed. Its causes include environmental, genetic, and social factors, such as advancing parental age at conception. In my lab, we focus on the genetic causes of autism, particularly mutations in the SHANK3 gene. This gene is vital for the protein that binds receptors in neurons, essential for receiving chemical signals that enable neuron communication. Damage to SHANK3 can disrupt this communication, impairing brain development and function. Our study aims to explore previously unknown mechanisms through which SHANK3 mutations affect brain development, leading to autism.”
Specifically, the research team focused on two components in the brain that have not yet been studied extensively in this context: non-neuronal brain cells (glia) called oligodendrocytes and the myelin they produce. Myelin tissue is a fatty layer that insulates nerve fibres (axons), similar to the insulating layer that coats electrical cables. When the myelin is faulty, the electrical signals transmitted through the axons may leak, disrupting the message transmission between brain regions and impairing brain function.
The team employed a genetically engineered mouse model for autism, introducing a mutation in the Shank3 gene that mirrors the mutation found in humans with this form of autism. Inbar Fischer: “Through this model, we found that the mutation causes a dual impairment in the brain’s development and proper function: first, in oligodendrocytes, as in neurons, the SHANK3 protein is essential for the binding and functioning of receptors that receive chemical signals (neurotransmitters and others) from neighbouring cells. This means that the defective protein associated with autism disrupts message transmission to these vital support cells. Secondly, when the function and development of oligodendrocytes is impaired, their myelin production is also disrupted. The faulty myelin does not properly insulate the neuron’s axons, thereby reducing the efficiency of electrical signal transmission between brain cells and the synchronization of electrical activity between different brain parts. In our model, we found myelin impairment in multiple brain areas and observed that the animals’ behaviour was adversely affected.”
The researchers then sought a method for fixing the damage caused by the mutation, hoping to develop a treatment for humans ultimately. Inbar Fischer: “We obtained oligodendrocytes from the brain of a mouse with a Shank3 mutation and inserted DNA segments containing the normal human SHANK3 sequence. Our goal was to allow the normal gene to encode a functional and normal protein, which would perform its essential role in the cell by replacing the defective protein. To our delight, following treatment, the cells expressed the normal SHANK3 protein, enabling the construction of a functional protein substrate to bind the receptors that receive electrical signals. In other words, the genetic treatment we had developed repaired the oligodendrocytes’ communication sites, essential for the cells’ proper development and function as myelin producers.”
To validate findings from the mouse model, the research team generated induced pluripotent stem cells from the skin cells of a girl with autism caused by a SHANK3 gene mutation identical to that in the mice. From these stem cells, they derived human oligodendrocytes with the same genetic profile. These oligodendrocytes displayed impairments similar to those observed in their mouse counterparts.
Prof. Barak concludes: “In our study, we discovered two new brain mechanisms involved in genetically induced autism: damage to oligodendrocytes and, consequently, damage to the myelin they produce. These findings have important implications – both clinical and scientific. Scientifically, we learned that defective myelin played a significant role in autism and identified the mechanism causing the damage to myelin. Additionally, we revealed a new role for the SHANK3 protein: building and maintaining a functional binding substrate for receptors critical for message reception in oligodendrocytes (not just in neurons). We discovered that contrary to the prevailing view, these cells play essential roles in their own right, far beyond the support they provide for neurons — often seen as the leading players in the brain. In the clinical sphere, we validated a gene therapy approach that led to significantly improved development and function of oligodendrocytes derived from the brains of mice modelling autism. This finding offers hope for developing genetic treatment for humans, which could enhance the myelin production process in the brain. Furthermore, recognizing the significance of myelin impairment in autism—whether linked to the SHANK3 gene or not—opens new pathways for understanding the brain mechanisms underlying autism and paves the way for future treatment development.
Join me to discuss a specific MS drug shown in research thus far to help with remyelination! Do you remember that there was research in the MS world that looked at the possible effects of clemastine on MS? That same research has been integral in helping researchers develop an even more effective drug currently in phase two trials, and it’s showing promising results for remyelination in humans!
In this study, I review data from an article that examines 61 randomized trials involving 46,611 participants. The focus is on identifying the predictors of who is more likely to experience relapses and new MRI lesions. I also explore which individuals benefit the most from medications and discuss the associated risks.
Adults diagnosed with type 2 diabetes in mid-life—before age 50—are more likely to develop dementia.
Individuals diagnosed with type 2 diabetes at a younger age face a greater risk of developing dementia compared to those diagnosed later in life, according to research conducted by experts at the NYU Rory Meyers College of Nursing.
“Our study indicates that early-onset type 2 diabetes may have cognitive consequences. It highlights the need for prevention strategies for dementia that take both diabetes and obesity into account,” said Xiang Qi, assistant professor at NYU Meyers and the study’s lead author.
Type 2 diabetes is a recognized risk factor for dementia. While the exact mechanisms behind this connection are not completely understood, researchers believe that certain characteristics of diabetes—such as high blood sugar levels, insulin resistance, and inflammation—may contribute to the onset of dementia in the brain.
Type 2 diabetes, once common among older adults, is now increasingly seen in younger individuals. Currently, one in five people with type 2 diabetes globally is under 40 years old.
To investigate how the timing of a type 2 diabetes diagnosis is associated with the risk of developing dementia, a research team analyzed data from the Health and Retirement Study, conducted by the University of Michigan Institute for Social Research. The study, published in PLOS ONE, included 1,213 U.S. adults aged 50 and older who had type 2 diabetes confirmed by blood tests and did not have dementia when they entered the study. The participants were followed for up to 14 years, during which 216 individuals (17.8%) developed dementia, as determined by follow-up telephone interviews.
The researchers found that adults diagnosed with type 2 diabetes at younger ages were at increased risk for developing dementia compared to those diagnosed at 70 years or older. Adults diagnosed with diabetes before age 50 were 1.9 times as likely to develop dementia as those diagnosed at 70 and older, while those diagnosed between 50-59 years were 1.72 times as likely and those diagnosed between 60-69 years were 1.7 times as likely.
Using linear trend tests, the researchers found a graded association between age at diagnosis and dementia risk: for each year younger a person is at the time of their type 2 diabetes diagnosis, their risk for developing dementia increases by 1.9%.
“While we do not know for sure why an earlier diabetes diagnosis would increase the risk for dementia, prior studies show that people diagnosed with type 2 diabetes in mid-life may experience more vascular complications, poor blood sugar control, and insulin resistance—all of which are known risk factors for cognitive impairment,” said Bei Wu, the Dean’s Professor in Global Health and vice dean for research at NYU Meyers and the study’s senior author.
In addition, obesity appeared to influence the relationship between type 2 diabetes and dementia. Individuals with obesity who were diagnosed with type 2 diabetes before age 50 had the highest dementia risk in the study.
The researchers note that this greater understanding of the connection between diabetes onset, obesity, and dementia may help inform targeted interventions to prevent dementia.
“Our study highlights the importance of one’s age at diabetes diagnosis and suggests that specifically targeting obesity—whether through diet and exercise or perhaps medication—may play a role in staving off dementia in younger adults with diabetes,” said Wu.
We use cookies on our website to give you the most relevant experience by remembering your preferences and repeat visits. By clicking “Accept”, you consent to the use of ALL the cookies.
This website uses cookies to improve your experience while you navigate through the website. Out of these, the cookies that are categorized as necessary are stored on your browser as they are essential for the working of basic functionalities of the website. We also use third-party cookies that help us analyze and understand how you use this website. These cookies will be stored in your browser only with your consent. You also have the option to opt-out of these cookies. But opting out of some of these cookies may affect your browsing experience.
Necessary cookies are absolutely essential for the website to function properly. This category only includes cookies that ensures basic functionalities and security features of the website. These cookies do not store any personal information.
Any cookies that may not be particularly necessary for the website to function and is used specifically to collect user personal data via analytics, ads, other embedded contents are termed as non-necessary cookies. It is mandatory to procure user consent prior to running these cookies on your website.
We use cookies to ensure that we give you the best experience on our website. If you continue to use this site we will assume that you are happy with it.OkNo
