Search Index

Implementing established physical theories into the constructions of the future Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Building Physics Last updated: 03/04/25, 10:39 Published: 20/02/25, 08:00 Implementing established physical theories into the constructions of the future From the high rise establishments that paint the expansive London skyline to the new build properties nestled within thriving communities, buildings serve as a beacon of societal needs. The planned and precise architecture of buildings provides shelter and comfort for individuals, as well as meet business agendas to promote modern day living. Additionally, buildings serve a purpose as a form of protection where, according to the World Health Organisation (WHO), the design and construction of buildings is to create an environment suitable for human living: more favourable than the state of the natural environment outdoors construction and building protects us from: extremes of temperature moisture excessive noise To sustain these pivotal agendas, a comprehensive analysis of the physical factors within the environment of buildings, including temperature, light and sound are required for design and legislation for a building to function. The field of ‘Building Physics’ primarily addresses these physical factors to innovate ‘multifunctional solutions’, be more efficient, and build upon present designs, which can be adapted for future use. Moreover, the built environment is regarded as one of the biggest carbon emissions on the planet, so using building physics as an early design intervention can reduce energy consumption and minimise carbon emissions. This supports global manifestos of moving towards net zero and decreasing the likelihood of the detrimental effects caused by climate change. The main components of Building Physics Building Physics is composed of examining the functions of an interior physical environment, including air quality, thermal comfort, acoustics comfort (sound), and light : Air quality: Ventilation is needed for maintaining a safe environment and reducing the quantity of stale air - consisting of carbon dioxide and other impurities - within an interior environment. Air infiltration also contributes to a significant heat loss, where it is important to provide intentional ventilation to increase the efficiency of energy transfers within the building. Thus, good ‘airtightness’ of a building fabric, which can be considered as the building’s resistance to unintentional air infiltration or exfiltration, can enable planned airflows for ventilation. Thermal: The biggest influence within the field of Building Physics stems from an understanding of heat conductivity depending on the density and moisture content of the material, as well as heat transfers - conduction, convection, radiation and transition - to determine the suitability of materials used for construction. For example, a material such as a solid wood panel for walls and ceilings is favourable as it can be installed in layers, providing even temperature fields across the surface. It is important that a building has the ability to isolate its environment from external temperature conditions and have the correct building envelope - a barrier that separates the interior and exterior of a building. Acoustics: A regulated control of sound within buildings contributes towards maintaining habitable conditions for building users to make sure that sound is loud, undistorted, and the disturbances are reduced. Acoustics can be controlled and modified through material choices, such as installing sound-absorbing material. These materials can be adapted to reduce sound leakage, which are common in air openings, such as ventilators and doors, that are more likely to transmit sound than adjacent thicker walls. Light: Light provides an outlook of viewing an environment in an attractive manner, particularly using daylight as a primary source of enhancing the exterior of a building, whilst also functioning within a building. One strategy used to fulfil the purpose of light in buildings is designing windows for the distribution of daylight to a space. The window design has a divisive effect on the potential daylight and thermal performance of adjacent spaces, so it needs to be closely checked using the standardised methods, in order to be suitable for use. Additionally, as windows are exposed to the sky, daylighting systems can adapt windows to transmit or reflect daylight as a function of incident angle, for solar sharing, protection from glare and redirection of daylight. Overall, a key objective of sustaining a safe and eco-friendly building is to ensure that the space has proper heat and humidity aligning with a suitable degree of acoustic and visual comfort in order to sustain the health of the people using the building. Particularly within modern society, a combination of Building Physics principles and digitalised software, such as Building Information Modelling (BIM), can enhance the design process of a building to provide healthy environments for generations to come. Written by Shiksha Teeluck Related article: Titan Submersible REFERENCES Unsplash. A construction site with cranes [Internet]. [Accessed 2 January 2025]. Available from: https://unsplash.com/photos/a-construction-site-with-cranes-mOA2DAtcd1w . Katunský D, Zozulák M. Building Physics . 2012. ISBN: 978-80-553-1261-3. Partel. Building Physics [Internet]. [Accessed 2 January 2025]. Available from: https://www.partel.co.uk/resources/building-physics/#:~:text=According%20to%20WHO%20(World%20Health,%3A%20in%20contrast%2C%20allows%20productions . RPS Group. A day in the life of a senior building physics engineer [Internet]. [Accessed 4 January 2025]. Available from: https://www.rpsgroup.com/insights/consulting-uki/a-day-in-the-life-of-a-senior-building-physics-engineer/ . Cyprus International University. What is Building Physics and Building Physics Problems in General Terms [Internet]. [Accessed 6 January 2025]. Available from: /mnt/data/What_Is_Building_Physics_and_Building_Ph.pdf. Centre for Alternative Technology. Airtightness and Ventilation [Internet]. [Accessed 6 January 2025]. Available from: https://cat.org.uk/info-resources/free-information-service/eco-renovation/airtightness-and-ventilation/#:~:text=With%20good%20airtightness%2C%20effective%20ventilation,won't%20work%20as%20intended . KLH. Building Physics [Internet]. [Accessed 6 January 2025]. Available from: https://www.klh.at/wp-content/uploads/2019/10/klh-building-physics-en.pdf . Watson JL. Climate and Building Physics [Internet]. [Accessed 6 January 2025]. Available from: https://calteches.library.caltech.edu/98/1/Watson.pdf . Ruck N, Aschehoug Ø, Aydinli S, Christoffersen J, Edmonds I, Jakobiak R, et al. Daylight in Buildings - A source book on daylighting systems and components . 2000 Jun. Synergy Positioning Systems. How BIM Saves Time & Money for Construction Businesses [Internet]. [Accessed 6 January 2025]. Available from: https://groupsynergy.com/synergy-positioning-news/how-bim-saves-time-money-for-construction-businesses . Project Gallery

The effect on sleep on nutrition (nutrition timing) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The interaction between circadian rhythms and nutrition Last updated: 27/04/25, 11:20 Published: 01/05/25, 07:00 The effect on sleep on nutrition (nutrition timing) The circadian system regulates numerous biological processes with roughly a 24-hour cycle, helping the organism adapt to the day-night rhythm. Among others, circadian rhythms regulate metabolism, energy expenditure, and sleep, for which meal timing is an excellent inducer. Evidence has shown that meal timing has a profound impact on health, gene expression, and lifespan. Proper timed feeding in accordance with the natural circadian rhythms of the body might improve metabolic health and reduce chronic disease risk. Circadian rhythms Circadian rhythms are controlled by the central clock of the brain, which coordinates biological functions with the light-dark cycle. Along with meal timing, circadian rhythms influence key elements of metabolism such as insulin sensitivity, fat storage, and glucose metabolism. When meal timing is not synchronised with the body's natural rhythm, it can cause circadian misalignment, disrupting metabolic processes and contributing to obesity, diabetes, and cardiovascular diseases. Literature has indicated that one should eat best during the daytime, particularly synchronised with the active phase of the body. Eating late at night or in the evening when the circadian rhythm of the body is directed towards sleep could impair metabolic function and lead to weight gain, insulin resistance, and numerous other diseases. Also, having larger meals in the morning and smaller meals later in the evening has been linked to improved metabolic health, sleep quality, and even lifespan. A time-restricted eating window, in which individuals eat all meals within a approximately 10–12 hour window, holds promise for improving human health outcomes like glucose metabolism, inflammation, harmful gene expression, and weight loss ( Figure 1 ). It is necessary to consider the impact of meal timing on gene expression. Our genes react to a number of stimuli, including environmental cues like food and light exposure. Gene expression of the body's metabolic, immune, and DNA repair processes are regulated by the body's circadian clock. Disturbances in meal timing influence the expression of these genes, which may result in greater susceptibility to diseases and reduced lifespan. Certain nutrients, such as melatonin in cherries and grapes, and magnesium in leafy greens and nuts, can improve sleep quality and circadian entrainment. Omega-3 fatty acids in fatty fish and flax seeds also have been shown to regulate circadian genes and improve metabolic functions. Other species Meal timing is quite varied among species, and animals have adapted such that food-seeking behavior is entrained into circadian rhythm and environmental time cues. There are nocturnal animals which eat at night, when they are active ( Figure 2 ). These nocturnal animals have evolved to align their meal time with their period of activity to maximise metabolic efficiency and lifespan. Meal timing is optimised in these animals for night activity and digestion. Humans, and most other animals, are diurnal and consume food during the day. In these animals, consuming most of their calories during the day is conducive to metabolic processes like glucose homeostasis and fat storage. These species tend to have better metabolic health when they are on a feeding regimen that is synchronized with the natural light-dark cycle. Conclusion Meal timing is important in human health, genetics, and life expectancy. Synchronising meal times with the body's circadian rhythms optimises metabolic function, reduces chronic disease incidence, and potentially increases longevity by reducing inflammatory genes and upregulating protective ones. This altered gene expression affects the way food is metabolised and metabolic signals are acted upon by the body. Humans naturally gravitate towards eating during daytime hours, while other creatures have feeding habits that are adaptively suited to their own distinct environmental needs. It is important to consider this science and incorporate it into our schedules to receive the best outcome from an activity that we do not normally think about. Written by B. Esfandyare Related article: The chronotypes REFERENCES Meléndez-Fernández, O.H., Liu, J.A. and Nelson, R.J. (2023). Circadian Rhythms Disrupted by Light at Night and Mistimed Food Intake Alter Hormonal Rhythms and Metabolism. International Journal of Molecular Sciences , [online] 24(4), p.3392. doi: https://doi.org/10.3390/ijms24043392 . Paoli, A., Tinsley, G., Bianco, A. and Moro, T. (2019). The Influence of Meal Frequency and Timing on Health in Humans: The Role of Fasting. Nutrients , [online] 11(4), p.719. Available at: https://www.ncbi.nlm.nih.gov/pubmed/30925707 . Potter, G.D.M., Cade, J.E., Grant, P.J. and Hardie, L.J. (2016). Nutrition and the circadian system. British Journal of Nutrition , [online] 116(3), pp.434–442. doi: https://doi.org/10.1017/s0007114516002117 . St-Onge MP, Ard J, Baskin ML, et al. Meal timing and frequency: implications for obesity prevention. Am J Lifestyle Med. 2017;11(1):7-16. Patterson RE, Sears DD. Metabolic effects of intermittent fasting. Annu Rev Nutr. 2017;37:371-393. Zhdanova IV, Wurtman RJ. Melatonin treatment for age-related insomnia. Endocrine. 2012;42(3):1-12. Prabhat, A., Batra, T. and Kumar, V. (2020). Effects of timed food availability on reproduction and metabolism in zebra finches: Molecular insights into homeostatic adaptation to food-restriction in diurnal vertebrates.Hormones and Behavior, 125, p.104820. Project Gallery

Broadening access for (black) women in STEM Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Power of sisterhood in STEM Last updated: 28/03/25, 11:10 Published: 28/03/25, 08:00 Broadening access for (black) women in STEM In collaboration with SiSTEM for International Women's Month Entering a fluid dynamics lecture. Looking under a microscope confined to the four walls of a lab. Walking onto a construction site or a board meeting. As a woman in these spaces, particularly as a woman of colour it is easy to believe you are the ONLY one. That’s what we thought, two sisters of black heritage starting out in the biomedical and the engineering field respectively. The higher we went in education the less people that looked like us. Being 1 of 10 women in a cohort of 200 was a familiar sight. Being less than 2% of the engineering workforce as a woman, you can start to feel like science, technology, engineering and maths (STEM) is not for you. But the reality is there are women in STEM doing incredible work. STEM is not a man’s industry. As women, we deserve our space on the STEM table. Through our struggles and isolating experiences, we decided to create SiSTEM, a community for all these wonderful women. Real life sisterhood We are often asked how we find working with your sister. Truth is, we wouldn’t be each other’s first choice for a business partner! We never thought we would start an organisation together, growing up as most siblings we have always wanted to do our own thing. Science and engineering was always seen as us doing separate things. Moreover we have completely different personalities. But we are two sisters with one dream; we don’t want another girl to leave the STEM field because she doesn’t believe she belongs there. We don’t want another girl to disqualify herself from her STEM career or degree because she has been told she doesn’t have the look for STEM or grades to do well. We have one passion and that’s to change the narrative of women in STEM, particularly black women and those from lower socioeconomic backgrounds. There is power in numbers Community and having a support system are important. We wouldn’t have completed our STEM degrees or broken into our careers without our personal sisterly support. We were always a phone call away for each other, ready to be a listening ear and a cheerleader. That same sisterly support is what we offer to other women and girls through our initiative. There’s power in sisterhood, standing on the shoulders of great women. Women face unique challenges particularly in the STEM industry, discrimination, feeling less valued, difficulty with pay and promotion but by building a culture of support we empower women to thrive despite the barriers. It’s beautiful to belong to a circle of women as we are stronger together. By belonging to a community it cultivates a feeling of belonging. You also learn from one another, sparking interesting conversations, building important connections. We learn from our community everyday: the conversations we are able to have inspire us and broaden our knowledge. Throwing the rope to the next generation From its inception, SiSTEM’s goal was to support women and girls throughout their STEM journey. The gender gap issue in STEM starts very early on, very often not when we choose our degree courses but as early as primary school. That’s why we empower young girls as young as five years old. Every girl, every woman deserves to be part of a community. Every stage of the journey has its unique challenges which belonging to community can help navigate. I’m sure you’ve heard the saying ‘empowered women empower women’ - now we feel empowered to empower other girls and women. We originally felt like we were not the people to create this community. Imposter syndrome told us we weren’t qualified enough, that we didn’t have a story to tell worth listening to. Reflecting on our own journeys, it’s women like our teachers, our mother, our friends who have been key in our success. Our mum telling us to ‘aim high and be the best’, a female science teacher telling us ‘you can be whatever you want to be’, a friend's comment on our graduation post saying how proud they are. And now a community of women who we can lean on for support, receive advice and inspire us every day. Today, we meet women at schools, events, universities and workplaces. A common theme in some of these women and girls we meet is a lack of confidence. Our biggest joy is when we are able to put a smile on a young girl’s face who feels giving up.Women need reminding how amazing they are so we continue to do amazing things, find a cure for cancer, make an innovative product to solve the world’s biggest problems or to design a beautiful building which would will be seen by generations to come. We shouldn’t be afraid to share our personal stories of how we got to where we are. when others hear they are empowered. This is what we use our platform to do. We are able to pass on the mic to other woman to share their untold stories. By putting a light on various women particularly black women in STEM we are giving others positive roles models to look to where they able to believe they do can do it. An empowered woman is a force of nature. She shines. She encourages. She breaks barriers and has the confidence to speak up in a place where she was told to be silent. By forming our community even though we may still find that we are the only women in the room, we have many women standing behind us and many more coming. Conclusion Retention of women in STEM is as equally as important as getting women into STEM. There is a leaky pipeline particularly between university level and STEM leadership positions and also many young girls already have a negative perception about certain STEM careers. That’s why we created an initiative to encourage more girls to get into STEM through innovative workshops and outreach programs and to create a community for women currently in the field. By doing so we aim to open the bottle top at one end and close any holes at the other end. Women supporting women in a powerful thing and there is space for all women in stem, no matter your background, academic records or skin colour. Together we make STEM colourful…preferably pink! -- Scientia News wholeheartedly thanks SiSTEM for this important piece on female representation in STEM. We hope you enjoyed reading this International Women's Month Special piece! For more information, check them out on Instagram and LinkedIn . -- Related articles: Representation in STEM / Women leading in biomedical engineering / African-American women in cancer research Project Gallery

Research shows that insomnia does have a hereditary side Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Does insomnia run in families? Here's what genetics tells us Last updated: 10/07/25, 18:25 Published: 10/07/25, 18:11 Research shows that insomnia does have a hereditary side Have you ever noticed restless nights affecting more than one relative? Maybe your sister tosses and turns, or your brother wakes up before dawn, wide awake and anxious. It might feel like poor sleep is passed down from parents to kids, and science suggests that feeling isn’t just in your head. In one study, nearly 40% of people with insomnia had a close family member with it, compared to 29% of those without; making them 1.57 times more likely to share the struggle. So is that inherited, or just a string of bad luck? Here’s what science has to say. Your DNA can affect sleep Research shows that insomnia does have a hereditary side. If someone in your family, say a parent, sibling or even a grandparent, struggles night after night, you’re more likely to face similar problems. That doesn’t guarantee you’ll wake up at 3 a.m. every night, but it does raise your baseline risk: studies estimate that around one-third of insomnia liability is genetic. In practical terms, inheriting certain gene variants can make the brain’s sleep-promoting signals weaker or the wake-promoting signals stronger. Think of those genes as nudging you toward more restless nights rather than pushing you entirely into insomnia. So if genes only lay the groundwork, what else determines whether someone actually stays awake counting sheep? That’s where life’s daily stresses come into play. How genes shape your sleep Scientists have identified a handful of genes that guide our body’s natural clock. Our circadian rhythm influences how deeply and how long we sleep. For instance, variants in the PER3 or CLOCK genes can shift your internal timing. This makes it harder to feel sleepy at a conventional hour. Picture the circadian clock as an orchestra conductor: if the conductor’s timing fluctuates, the entire performance, your sleep cycle, can fall out of sync. Other inherited factors affect the brain’s “volume knobs” for alertness. Certain gene differences can heighten sensitivity to minor disturbances; like a creaky floorboard or an ambulance siren, so that you jitter awake even when there’s no real threat. Over time, those tiny awakenings add up, preventing you from reaching the deep, restorative stages of sleep. Yet, these genes don’t act in isolation. The brain remains remarkably adaptable through epigenetic changes; chemical tags that turn genes on or off. Experiences such as stress, illness, or a drastically changed schedule can strengthen or weaken those genetic susceptibilities. Sleep isn’t just genetic; here’s why Even if you inherit gene variants linked to insomnia, your environment and habits often decide the end result. High-pressure jobs, financial worries, or family conflicts can ignite sleep troubles in someone without a family history of insomnia. Conversely, someone with a strong genetic vulnerability might sleep soundly if life stays relatively stress-free and routines remain consistent. Everyday choices, like scrolling through social media until the last minute, drinking coffee late afternoon, or keeping wildly shifting bedtimes, further fuel the problem. For example, evening exposure to bright screens suppresses melatonin, the hormone that signals your brain it’s time to sleep. That means even if your “insomnia genes” are mild, you’re still creating obstacles to a good night’s rest. On the other hand, regular exercise (aim for at least 30 minutes most days), a balanced diet, and a calm, screen-free wind-down routine signal the brain that it’s safe to switch off. Over months, those good habits can overwrite the nudge from your genes, steering you towards deep, uninterrupted rest. Can you change your genetic destiny? Knowing that insomnia has a genetic component can feel validating. It clarifies that tossing and turning isn’t simply an unexplained routine. That awareness reduces shame and makes it easier to adopt practical solutions. If you suspect poor sleep runs in your family, watch for early warning signs: difficulty falling asleep, waking often, or waking too early. Catching these patterns early means you can experiment with sleep hygiene tweaks before the problem becomes chronic. Actionable steps include setting a consistent bedtime, dimming lights an hour before sleep, avoiding caffeine after mid-afternoon, and practising relaxation techniques, such as deep breathing or progressive muscle relaxation. If these changes don’t help, cognitive behavioural therapy for insomnia (CBT-I) targets both the thoughts and behaviours that perpetuate sleeplessness, effectively retraining the brain’s response to the bedroom. Those inherited sleep tendencies might suggest insomnia is written in your DNA; but by keeping a consistent bedtime, cutting down on late-night screens and being kind to yourself, you can rewrite that genetic script and finally enjoy the deep rest you’ve earned. Written by Rand Alanazi Related articles: Does anxiety run in families? / Link between sleep and memory loss / The chronotypes REFERENCES Beaulieu-Bonneau S, LeBlanc M, Mérette C, Dauvilliers Y, Morin CM. Family History of Insomnia in a Population-Based Sample. Sleep. 2007 Dec;30(12):1739–45. Pacheco D. Is Insomnia Genetic? [Internet]. Sleep Foundation. 2021. Available from: https://www.sleepfoundation.org/insomnia/is-insomnia-genetic PER3 [Internet]. Wikipedia. 2023. Available from: https://en.wikipedia.org/wiki/PER3 Dashti HS, Jones SE, Wood AR, Lane JM, van Hees VT, Wang H, et al. Genome-wide association study identifies genetic loci for self-reported habitual sleep duration supported by accelerometer-derived estimates. Nature Communications [Internet]. 2019 Mar 7;10(1):1–12. Available from: https://www.nature.com/articles/s41467-019-08917-4 Halperin D. Environmental noise and sleep disturbances: A threat to health? Sleep Science [Internet]. 2014 Dec;7(4):209–12. Available from: https://www.sciencedirect.com/science/article/pii/S1984006314000601 www.ushealthconnect.com H. Unraveling the Impact of Environmental Factors on Sleep Quality and Parkinson Disease [Internet]. Practicalneurology.com . 2025. Available from: https://practicalneurology.com/diseases-diagnoses/movement-disorders/unraveling-the-impact-of-environmental-factors-on-sleep-quality-and-parkinson-disease/32197/ Levenson JC, Kay DB, Buysse DJ. The Pathophysiology of Insomnia. Chest [Internet]. 2015 Apr;147(4):1179–92. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC4388122/ Spielman AJ, Caruso LS, Glovinsky PB. A Behavioral Perspective on Insomnia Treatment. Psychiatric Clinics of North America [Internet]. 1987 Dec 1;10(4):541–53. Available from: https://www.sciencedirect.com/science/article/pii/S0193953X1830532X the I. amBX [Internet]. amBX. 2020 [cited 2025 Jun 6]. Available from: https://www.ambx.com/news/what-is-the-natural-circadian-rhythm Hassell K, Reiter RJ, Robertson NJ. MELATONIN AND ITS ROLE IN NEURODEVELOPMENT DURING THE PERINATAL PERIOD: A REVIEW. Fetal and Maternal Medicine Review. 2013 May 1;24(2):76–107. Wang J, Liu J, Xie H, Gao X. Effects of Work Stress and Period3 Gene Polymorphism and Their Interaction on Sleep Quality of Non-Manual Workers in Xinjiang, China: A Cross-Sectional Study. International Journal of Environmental Research and Public Health. 2022 Jun 3;19(11):6843–3. Project Gallery

Famine-induced epigenetic changes and public health strategies in affected populations Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why South Asian genes remember famine Last updated: 18/09/25, 08:44 Published: 23/01/25, 08:00 Famine-induced epigenetic changes and public health strategies in affected populations Our genes are often thought of as a fixed blueprint, but what if our environment could change how they work? This is the intriguing idea behind epigenetics—a field that shows how our environment, combined with the body’s adaptive responses for survival, can influence gene expression without altering our DNA. In South Asia, famines such as the infamous Bengal Famine of 1943 caused immense suffering, and these hardships may have triggered genetic changes that continue to affect generations. Today, South Asians face an increased risk of developing Type 2 diabetes by age 25, whereas White Europeans generally encounter this risk around age 40. What is driving this difference in risk? This article will explore the science behind these epigenetic changes, their impact on the descendants of famine survivors and how these insights can shape public health, policy, and research. The legacy of historical famines In 1943, the Bengal Famine claimed around three million lives. Nobel laureate Amartya Sen argues that the severity of the famine was not merely a result of prior natural disasters and disease outbreaks in crops. Instead, it was primarily driven by wartime inflation, speculative buying, and panic hoarding, which disrupted food distribution across the Bengal region. Consequently, for the average Bengali citizen, death from starvation, disease, and malnutrition became widespread and inevitable. The impact of the famine extended well beyond the immediate loss of life. Dr Mubin Syed, a radiologist specialising in vascular and obesity medicine, emphasises that these famines have left a lasting mark on the health of future generations. Dr Syed explains that South Asians, having endured numerous famines, have inherited "starvation-adapted" traits. These traits are characterised by increased fat storage. As a result, the risk of cardiovascular diseases, diabetes, and obesity is heightened in their descendants. This tendency towards fat storage is believed to be closely tied to epigenetic factors, which play a crucial role in how these traits are passed down through generations. Epigenetic mechanisms and their impact These inherited traits are shaped by complex epigenetic mechanisms, which regulate gene expression in response to environmental stressors like famines without altering the underlying DNA sequence. DNA methylation, a process involving the addition of small chemical groups to DNA, plays a crucial role in regulating gene expression. When a gene is 'on,' it is actively transcribed into messenger RNA (mRNA), resulting in the synthesis of proteins such as enzymes that regulate energy metabolism or hormones like insulin that manage blood sugar levels. Conversely, when a gene is 'off,' it is not transcribed, leading to a deficiency of these essential proteins. During periods of famine, increased DNA methylation can enhance the body's ability to conserve and store energy by altering the activity of metabolism-related genes. Epigenetic inheritance, a phenomenon where some epigenetic tags escape the usual reprogramming process and persist across generations, plays a crucial role in how famine-induced traits are passed down. Typically, reproductive cells undergo a reprogramming phase where most epigenetic tags are erased to reset the genetic blueprint. However, certain DNA methylation patterns can evade this erasure and remain attached to specific genes in the germ cells, the cells that develop into sperm and egg cells. These persistent modifications can influence gene expression in the next generation, affecting metabolic traits and responses to environmental stressors. This means the metabolic adaptations seen in famine survivors, such as increased fat storage and altered hormone levels, can be transmitted to their descendants, predisposing them to similar health risks. Research has highlighted how these inherited traits manifest in distinct hormone profiles across different ethnic groups. A study published in Diabetes Care found that South Asians had higher leptin levels (11.82 ng/mL) and lower adiponectin levels (9.35 µg/mL) compared to Europeans, whose leptin levels were 9.21 ng/mL and adiponectin levels were 12.96 µg/mL. Leptin, encoded by the LEP gene, is a hormone that reduces appetite and encourages fat storage. Adiponectin, encoded by the ADIPOQ gene, improves insulin sensitivity and supports fat metabolism. Epigenetic changes, such as DNA methylation in the LEP and ADIPOQ genes, have led to these imbalances which were advantageous for South Asian populations during times of famine. Elevated leptin levels helped ensure the body could maintain energy reserves for survival, while lower adiponectin levels slowed fat breakdown, preserving stored fat for future use. This energy-conservation mechanism allowed individuals to endure long periods of food scarcity. Remarkably, these epigenetic changes can be passed down to subsequent generations. As a result, descendants continue to exhibit these metabolic traits, even in the absence of famine conditions. This inherited imbalance—higher leptin levels and lower adiponectin—leads to a higher predisposition to metabolic disorders. Increased leptin levels can cause leptin resistance, where the body no longer responds properly to leptin’s signals, driving overeating and fat accumulation. Simultaneously, reduced adiponectin weakens the body’s ability to regulate insulin and break down fats efficiently, resulting in higher blood sugar levels and greater fat storage. These combined effects heighten the risk of obesity and Type 2 diabetes in South Asian populations today. Integrating cultural awareness in health strategies Understanding famine-induced epigenetic changes provides a compelling case for rethinking public health strategies in affected populations. While current medicine cannot reverse famine-induced epigenetic changes in South Asians, culturally tailored interventions and preventive measures are crucial to reducing metabolic risks. These should include personalised dietary plans, preventive screenings, and targeted healthcare programmes. For example, the Indian Diabetes Prevention Programme showed that lifestyle changes reduced diabetes risk by 28.5% among high-risk individuals. Equally, policymakers must consider the broader societal factors that contribute to these health risks, and qualitative studies highlight challenges in shifting cultural attitudes. Expectations that women prepare meals in line with traditional norms often limit healthier dietary options.Differing perceptions of physical activity can complicate efforts to promote healthier lifestyles. For example, a study in East London found that some communities consider prayer sufficient exercise, which adds complexity to changing attitudes. Facing our past to secure a healthier future As we uncover the long-term effects of environmental stressors like historical famines, it becomes clear that our past is not just a distant memory but an active force shaping our present and future health. Epigenetic changes inherited from South Asian ancestors who endured famine have heightened the risk of metabolic disorders in their descendants. For instance, UK South Asian men have been found to have nearly double the risk of coronary heart disease (CHD) compared to White Europeans. Consultant cardiologist Dr Sonya Babu-Narayan has stated, “Coronary heart disease is the world’s biggest killer and the most common cause of premature death in the UK.” With over 5 million South Asians in the UK alone, this stark reality requires immediate action. We must not only address the glaring gaps in scientific research but also develop targeted public health policies to tackle these inherited health risks. These traits are not relics of the past; they are living legacies that, without swift intervention, will continue to affect generations to come. To truly address the inherited health risks South Asians face, we must go beyond surface-level awareness and commit to long-term, systemic change. Increasing funding for research that directly focuses on the unique health challenges within this population is non-negotiable. Equally crucial are culturally tailored public health initiatives that resonate with the affected communities, alongside comprehensive education programmes that empower individuals to take control of their health. These steps are not just about improving outcomes—they’re about breaking a cycle. The question, therefore, is not simply whether we understand these epigenetic changes, but whether we have the resolve to confront their full implications. Can we muster the political will needed to confront these inherited risks? Can we unite our efforts to stop these risks from affecting the health of entire communities? The cost of inaction is not just measured in statistics—it will be felt in the lives lost and the potential unrealised. The time to act is now. Written by Naziba Sheikh Related articles: Epigenetics / Food deserts and malnutrition / Mental health in South Asian communities / Global health injustices- Kashmir , Bangladesh REFERENCES Safi, M. (2019). Churchill’s policies contributed to 1943 Bengal famine – study. [online] the Guardian. Available at: https://www.theguardian.com/world/2019/mar/29/winston-churchill-policies-contributed-to-1943-bengal-famine-study . Bakar, F. (2022). How History Still Weighs Heavy on South Asian Bodies Today. [online] HuffPost UK. Available at: https://www.huffingtonpost.co.uk/entry/south-asian-health-colonial-history_uk_620e74fee4b055057aac0e9f . Sayed, M., Deek, F. and Shaikh, A. (2022). The Susceptibility of South Asians to Cardiometabolic Disease as a Result of Starvation Adaptation Exacerbated During the Colonial Famines. [online] Research Gate. Available at: https://www.researchgate.net/publication/366596806_The_Susceptibility_of_South_Asians_to_Cardiometabolic_Disease_as_a_Result_of_Starvation_Adaptation_Exacerbated_During_the_Colonial_Famines#:~:text=This%20crisis%20could%20be%20the,adapted%20physiology%20can%20become%20harmful . Utah.edu . (2009). Epigenetics & Inheritance. [online] Available at: https://learn.genetics.utah.edu/content/epigenetics/inheritance/ . Palaniappan, L., Garg, A., Enas, E., Lewis, H., Bari, S., Gulati, M., Flores, C., Mathur, A., Molina, C., Narula, J., Rahman, S., Leng, J. and Gany, F. (2018). South Asian Cardiovascular Disease & Cancer Risk: Genetics & Pathophysiology. Journal of Community Health, 43(6), pp.1100–1114. doi: https://doi.org/10.1007/s10900-018-0527-8 . Diabetes UK (2022). Risk of Type 2 Diabetes in the South Asian Community. [online] Diabetes UK. Available at: https://www.diabetes.org.uk/node/12895 . King, M. (2024). South Asian Heritage Month: A Journey Through History and Culture . [online] Wearehomesforstudents.com . Available at: https://wearehomesforstudents.com/blog/south-asian-heritage-month-a-journey-through-history-and-culture . Project Gallery

Beyond sugarcane fields and dreamy beaches, Mauritius secures first place in mobile connectivity Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Mauritius's rise as African leader of mobile networks Last updated: 08/06/25, 11:12 Published: 05/06/25, 07:00 Beyond sugarcane fields and dreamy beaches, Mauritius secures first place in mobile connectivity Background: GSMA ranking In the bustling capital city of Port Louis, commuters check the latest news updates using mobile data on their phones. Across the busy, connecting streets, a handful of tourists video call their family back home, asking them what souvenirs they would like- also on mobile data. Apart from idyllic holiday scenes and solid sugar exports, the island nation of Mauritius has recently become number one in Africa for mobile connectivity- as scored by the Global System for Mobile Communications Association (GSMA). The small island is now at the forefront of telecommunication development, with the increasing rollout of 5G networks. How did this touristic country become a leader in mobile connectivity? On the 13th of August 2024, the GSMA announced its yearly index for mobile connectivity. The GSMA looks at 41 African countries and ranks them based on: internet accessibility, prices of mobile devices, relevant services and political environments. Scoring 62.7 points out of the possible 100, Mauritius took the first spot, in front of South Africa. This result also places the island country 76th in the world. Remarkably, this is the third consecutive year that Mauritius is leading in mobile connectivity in Africa. Moreover Mauritius, with a population of 1.26 million, boasts an average of 1.7 phones per person, compared to only 1.2 phones per person in the US (according to 2023 data). Connecting the island: 5G is nearly everywhere Three companies provide mobile phone networks on Mauritius island: Emtel, MTML (Chili) and state-owned My.t. At present, 5G is widely available in Mauritius, thanks to Emtel supplying it to approximately 80% of the island for both residential and commercial usage. Though Emtel is the biggest network in the country, My.t is the most popular provider currently, and it also offers 5G to its users. A closer look at 4G and 5G 3G (and 3G High-Speed Packet Access, HSPA), 4G (Long Term Evolution, LTE) and 5G are wireless mobile networks, where the ‘G’ in these networks means ‘generation’ and indicates the strength of the signal on the mobile device. Hence, each mobile network is an improvement since the last generation of network. These mobile networks aim for high quality, reliable communication, and are based on radio signals. Each generation has evolved to achieve this. Table 1 compares the differences between all of these networks. The original 1G network from 1979 used analogue radio signals, while subsequent network generations use digital radio signals. Table 1: A comparison of 2G, 3G, 4G and 5G mobile networks 2G 3G HSPA+ 4G LTE 5G Speed 64Kbps 8Mbps 50Mbps 10Gbps Bandwidth 30- 200 kHz 15- 20 MHz 100 MHz 30- 300 GHz Features Better quality video calls than before Can send and receive larger emails Higher speeds and capacities Much faster speeds and capacities; high resolution video streaming SMS and MMS Larger capacities Low cost per bit Low latency Interactive multimedia, voice, video Allows remote control of operations e.g. vehicles, robots, medical procedures It is evident from Table 1 that not only have speeds and capacities increased with each generation, but new features have also been implemented such as video calls, interactive multimedia, streaming, and remote control of operations. Introduced in 2019, 5G is thought to be the most ambitious mobile phone network- almost revolutionary in its benefits since 1G. Usually, mobile carriers operate on a 4G LTE and 5G coexistence. This means that 5G phones can switch to 4G if 5G isn’t available in the region. Top of the tower- how? Since the 5G rollout in 2021, Mauritius has been enjoying the larger capacities and speeds of the network. The same question arises: how did this touristic country become a leader in mobile connectivity? There are several factors: - Tourist hotspot - Government initiatives - Improving local infrastructure - General advancements in mobile network technologies - High penetration rates and mobile ownership - Increasing number of connections - Geography Each factor will be considered in turn. Factor 1- Tourist hotspot Every year, Mauritius attracts visitors far and wide to enjoy its mesmerising beaches, luscious escapes and tantalising wildlife. Therefore, over time, mobile network technology has had to improve to meet the communicative needs of tourists. Put differently, tourism significantly supports the telecom industry on the island. Factor 2- Government initiatives As well as providing free, public WiFi hotspots around the island, the government is committed to bridging the digital divide and increasing access to all of its population. Thus, it was announced that, eligible citizens between the ages of 18 and 25 will receive a free, monthly mobile data package (with 4G and 5G capabilities)- starting from the 1st of September 2024. It is an endeavour to include young people in the government’s digital plans, i.e. digital inclusion. Factor 3- Improvements in local infrastructure In recent years, My.t and EmTel have been upgrading their equipment to ensure better coverage and access to 5G in the country. Infrastructure must have improved so that the three mobile operators on the island were granted the license for 5G rollout in June 2021. The current goal is to fully expand 5G coverage in Mauritius. Factor 4- General advancements in mobile network technologies Since its inception in 2019, 5G has had a profound impact on consumers around the globe with its low latency, high resolution streaming, and insanely high speeds and capacities. This pioneering mobile network has rolled out to millions of people, including the citizens of Mauritius island. The government has utilised this new technology to empower its people and pave a way for the country to become a leader in mobile connectivity. Factor 5- High penetration rates and mobile ownership Early 2025 data shows that the East African nation has over 2.1 million active mobile connections, when its population is half of that, a mere 1.261 million. (More mobile connections is not a usual thing as people may have separate connections for personal and work use, for example. Embedded SIMs – eSIMs- have made this possible recently). With this statistic, Mauritius has a high degree of mobile ownership and network connection density. Factor 6- An increase in the number of connections Another recent event is that the number of mobile connections in the nation has been increasing gradually: between 2024 and 2025, the number has increased by 1.9%. Factor 7- Geography It is known that less land- especially less rural land- makes deployment of cell phone towers and installation of masts much easier. Therefore, spanning an area of 2,040 squared kilometres, the main island of Mauritius can enjoy adequate mobile coverage- being one of the smallest African countries. Small island, big signal. To summarise, the above factors contribute to the number one ranking in mobile connectivity for Mauritius. What does Mauritius’s rise mean for the future? If these advancements in infrastructure and technology continue on the island, then there is a brighter outlook for the future. 5G coverage in Mauritius is on its way to completion, ensuring all districts have access to the latest mobile network. Geography, government initiatives, improvements in infrastructure by mobile operators, high number of mobile connections and ownership, are some of the factors that enabled 5G rollout in Mauritius in the first instance. Mauritius is leading by example to the other countries in Africa and is additionally performing well on the global stage for mobile networks. This small island country, usually known for its exotic sights and sugarcane landscape, is quickly overtaking its African neighbours in the race to become the leader in mobile phone connectivity. Written by Manisha Halkhoree Related articles: The future of semiconductor manufacturing / Wireless electricity Project Gallery

New research suggests that the cause extends far beyond the nervous system Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can what we eat, breathe, and do for a living affect our Parkinson’s risk? Last updated: 21/03/25, 11:59 Published: 10/04/25, 07:00 New research suggests that the cause extends far beyond the nervous system Introduction Parkinson’s disease (PD) is the most prevalent movement disorder and the second most common neurodegenerative disorder worldwide. PD is best known for causing tremors and stiffness, but it’s much more than a movement disorder. It also affects mood and speech. While PD is caused by the loss of dopamine-producing neurons in the brain’s substantia nigra, new research suggests that its roots may extend far beyond the nervous system. Surprisingly, the gut microbiome – trillions of bacteria living in our digestive tract – may play a key role in both the development and prevention of PD. These microbes help regulate inflammation and support brain health by influencing microglia, the brain’s immune cells. Diet also seems to matter: a Mediterranean-style diet rich in fruits, vegetables, and healthy fats appears to lower PD risk, while smoking – despite its well-known dangers – has been linked to a puzzling protective effect, possibly due to nicotine’s impact on the brain. Meanwhile, specific jobs, like farming, may increase PD risk due to pesticide exposure, which has been associated with neurodegeneration. The idea that what we eat, breathe, and do for a living could shape our brain health is intriguing. As research continues to uncover these surprising links, it raises an important question: could simple lifestyle changes help protect against neurodegenerative diseases? Gut-Brain Axis The gut-brain axis (GBA) is a two-way communication network between the enteric nervous system of the gastrointestinal (GI) tract and the central nervous system, connecting emotions and cognition with the intestines’ functions. This involves the brain sending signals to the gut and vice versa, which happens through the vagus nerve, gut hormones and the gut microbiome, which can produce chemicals to impact brain activity. This usually explains why stress signals from the brain can influence the digestion of food, causing symptoms such as stomach pain, bloating or changes in bowel movements. Alternatively, signals travelling from the gut to the brain can be seen when we eat something that makes us feel sick – we naturally avoid that food and the place where we ate it. Gut dysbiosis can be triggered by multiple factors, including diet, antibiotic use, infection, inflammation, and chronic stress. Dysbiosis is the imbalance in the composition and activity of the microbiota (microorganisms present in the gut). It is considered a risk factor for PD, but is not a direct cause of it. Changes in the microbiota can induce metabolic changes, which can result in increased local and systemic inflammation in addition to increased permeability of the intestines, making the gut ‘leaky’. Additionally, this can cause increased harmful gut bacteria (such as E. coli or Salmonella ) as they leak through the intestinal lining, producing amyloid proteins which can travel to the brain and cause the accumulation of α-synuclein – a protein linked to neurodegenerative diseases such as PD. There is also a reduction in healthy gut bacteria – which usually produce short-chain fatty acids (SCFAs) such as butyrate – which reduce inflammation and protect the brain cells. Less SCFAs cause an increase in inflammation and loss of the neuroprotective effects of SCFAs. Increased inflammation can eventually cause the weakening of the gut lining and a cycle of worsening dysbiosis, increased inflammation and increased α-synuclein accumulation, which spreads to the brain. Furthermore, gut dysbiosis can decrease the efficacy of dopaminergic treatments, which may be used to treat PD. In gut dysbiosis, harmful bacteria can produce an enzyme called dopa-decarboxylase – which converts Levodopa (a drug used to treat PD) into dopamine within the intestines. Hence, less Levodopa reaches the bloodstream and the brain, where it primarily acts and is converted to dopamine. This results in less Levodopa being converted to dopamine within the brain, reducing the effectiveness of the treatment. Consequently, this leads to motor symptoms and impairments such as tremors, which is a characteristic symptom of PD. Can food protect the brain? Could your diet be influencing your brain health in ways you never imagined? Research suggests that what you eat might play a critical role in either protecting your brain from PD or increasing your risk. People who follow a Mediterranean diet (MD) – rich in olive oil, fish, fruits, vegetables, whole grains, and nuts – may have up to a 25% lower risk of developing PD. Interestingly, this protective effect appears stronger in younger individuals and those in the early stages of PD. So.. what makes the MD so powerful? Gut microbiome boost: the MD promotes beneficial gut bacteria while reducing harmful microbes, supporting overall brain health. Anti-inflammatory effects: fibre from plant-based foods fuels the gut microbiome, leading to the production of SCFAs, which reduce inflammation and may slow PD progression. Mitochondrial protection: compounds in the MD, such as polyphenols in olive oil and omega-3 fatty acids in fish, help repair and protect mitochondria – the powerhouses of our cells. This helps prevent brain cell damage and maintain dopamine function. Neural growth & repair: walnuts and omega-3s may support neuronal growth and reduce protein clumping, a hallmark of PD. On the other hand, a Western diet – high in processed foods, saturated fats, refined sugars, and excess salt – may increase the risk of developing and worsening PD symptoms. Foods commonly associated with faster PD progression include canned fruits and vegetables, soda, fried foods, beef, ice cream, and cheese. Why does this happen? Microbiome disruption: the Western diet fosters an imbalance in gut bacteria, leading to inflammation and potential brain damage. Gut leakiness and neuroinflammation: a diet high in unhealthy fats and low in fibre can damage the gut lining, allowing harmful substances to enter the bloodstream and trigger brain inflammation. Hormonal imbalance: key gut-derived hormones (GLP-1, GIP, and IGN) that help protect neurons are disrupted by poor diet but can be restored through healthier food choices. While diet alone cannot cure PD, growing evidence suggests it can modify the disease course. A diet rich in fibre, healthy fats, and plant-based foods supports gut health, reduces inflammation, and may protect neurons from degeneration. Understanding these diet-microbiome-brain interactions could open new doors to PD prevention and treatment – proving once again that food truly is medicine. The smoking paradox One of the most intriguing findings in PD research is that smokers appear to have a lower risk of developing the disease. Epidemiological studies consistently show that people who smoke are less likely to be diagnosed with PD compared to non-smokers. But why? Scientists believe that nicotine, a key compound in tobacco, may play a neuroprotective role by affecting dopamine-producing neurons – the same cells that are progressively lost in PD disease. Nicotine interacts with receptors in the brain that influence dopamine release, which could help protect these neurons from degeneration. However, clinical trials testing nicotine as a treatment for PD have not shown significant benefits, suggesting that other compounds in tobacco or alternative mechanisms might be involved. Some researchers propose that additional chemicals in cigarette smoke, such as monoamine oxidase inhibitors, antioxidants, or even carbon monoxide at low levels, might contribute to this protective effect. Others suggest that genetic factors or lifestyle differences between smokers and non-smokers could also explain the association. Despite this fascinating link, smoking is not a recommended strategy for preventing PD. The well-documented risks – including cancer, cardiovascular disease, and lung damage – far outweigh any potential benefit. Instead, scientists are investigating whether specific compounds found in tobacco could be harnessed for new treatments without the harmful effects of smoking itself. What about my job? Can your job affect your risk of developing PD? Some studies suggest that certain occupations – like farming – might increase the risk, while others find no clear connection. So, what’s the truth? Let’s break it down. Some research suggests that farmers are more likely to develop PD, possibly due to exposure to pesticides like paraquat and rotenone, which have been linked to brain cell damage. Additionally, heavy metals found in agricultural environments – such as lead and manganese – may contribute to brain inflammation and oxidative stress, both of which play a role in PD. Furthermore, certain metals, including iron, mercury, copper, and manganese, can build up in the brain over time. Scientists believe that long-term exposure could damage the neurons that produce dopamine. However, the exact link isn’t fully understood, and not everyone exposed to these metals develops PD. That said, not all studies agree. Some large-scale research has found no significant link between farming, pesticide exposure, heavy metals and PD risk. This means that while environmental factors might play a role, other things – like genetics, lifestyle, or how long and intensely someone is exposed – could be just as important. So.. should you worry? If you work in farming or are regularly exposed to pesticides and heavy metals, it might be a good idea to take precautions, like using protective equipment and following safety guidelines. However, more research is needed to fully understand how these exposures contribute to PD. For now, staying informed and taking steps to reduce unnecessary exposure to harmful chemicals is a smart approach. What can you do? While there’s no guaranteed way to prevent PD, research suggests that certain lifestyle choices may help reduce the risk. Here are some science-backed steps you can take: 1. Adopt a Mediterranean-style diet: eating a diet rich in whole, plant-based foods, healthy fats (like olive oil and nuts), and lean proteins has been linked to a lower risk of PD. The Mediterranean diet is packed with antioxidants and anti-inflammatory compounds that may help protect brain cells. 2. Stay active: regular exercise isn’t just good for your muscles and heart – it may also help maintain gut health and protect neurons. Activities like walking, swimming, or strength training have been associated with a reduced risk of PD and other neurodegenerative diseases. 3. Limit pesticide exposure: for those in agricultural or industrial settings, protective measures, such as wearing gloves and masks and following safety guidelines, can help reduce exposure to potentially harmful chemicals linked to PD. 4. Monitor gut health: emerging research suggests that the gut microbiome may play a key role in PD. While scientists are still exploring microbiome-targeted therapies, maintaining good gut health by eating fibre-rich foods, fermented foods (like yogurt and kimchi), and staying hydrated may support overall well-being. Conclusion The connection between diet, gut health, lifestyle, and PD is an exciting area of research. While we don’t yet have all the answers, it’s clear that healthy habits – such as eating well, staying active, and minimising harmful exposures – can support both brain and overall health. As science continues to uncover new insights, making informed choices today can help protect your well-being in the long run! Written by Joecelyn Kirani Tan, Hanin Salem, Devikka Sivashanmuganathan & Barayturk Aydin Related articles: TDP43 and Parkinsonism / Diabetes drug to treat Parkinson's REFERENCES Berthouzoz E, Lazarevic V, Zekeridou A, Castro M, Debove I, Aybek S, Schrenzel J, Burkhard PR, Fleury V. Oral and intestinal dysbiosis in Parkinson's disease. Rev Neurol (Paris). 2023 Nov;179(9):937-946. doi: 10.1016/j.neurol.2022.12.010. Epub 2023 Mar 16. PMID: 36934020. Bisaglia M. Mediterranean Diet and Parkinson's Disease. Int J Mol Sci. 2022 Dec 20;24(1):42. doi: 10.3390/ijms24010042. PMID: 36613486; PMCID: PMC9820428. Firestone JA, Lundin JI, Powers KM, Smith-Weller T, Franklin GM, Swanson PD, Longstreth WT Jr, Checkoway H. Occupational factors and risk of Parkinson's disease: A population-based case-control study. Am J Ind Med. 2010 Mar;53(3):217-23. doi: 10.1002/ajim.20788. PMID: 20025075; PMCID: PMC3299410. Gorell JM, Johnson CC, Rybicki BA, Peterson EL, Richardson RJ. The risk of Parkinson's disease with exposure to pesticides, farming, well water, and rural living. Neurology. 1998 May;50(5):1346-50. doi: 10.1212/wnl.50.5.1346. PMID: 9595985. hms.harvard.edu . (2017). The Gut and the Brain. [online] Available at: https://hms.harvard.edu/news-events/publications-archive/brain/gut-brain . Hrncir, T. (2022). Gut Microbiota Dysbiosis: Triggers, Consequences, Diagnostic and Therapeutic Options. Microorganisms, [online] 10(3), p.578. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC8954387/#:~:text=Dysbiosis%20can%20be%20caused%20by,food%20additives)%2C%20and%20hygiene .. Jackson A, Forsyth CB, Shaikh M, Voigt RM, Engen PA, Ramirez V, Keshavarzian A. Diet in Parkinson's Disease: Critical Role for the Microbiome. Front Neurol. 2019 Dec 10;10:1245. doi: 10.3389/fneur.2019.01245. PMID: 31920905; PMCID: PMC6915094. Johns Hopkins Medicine (2025). Can Environmental Toxins Cause Parkinson’s Disease? https://www.hopkinsmedicine.org/health/conditions-and-diseases/parkinsons-disease/can-environmental-toxins-cause-parkinson-disease Kwon, D. et al. (2024) ‘Diet and the gut microbiome in patients with parkinson’s disease’, npj Parkinson’s Disease , 10(1). doi:10.1038/s41531-024-00681-7. Physiopedia. (n.d.). Gut Brain Axis (GBA). [online] Available at: https://www.physio-pedia.com/Gut_Brain_Axis_(GBA) . Project Gallery

Rock-wallabies are adapted to occupy specific rocky habitats, like outcrops, cliffs and caves Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Protecting rock-wallabies in Australia Last updated: 06/11/25, 11:54 Published: 29/05/25, 07:00 Rock-wallabies are adapted to occupy specific rocky habitats, like outcrops, cliffs and caves This is the final article (article no. 7) in a series on animal conservation. Previous article: Emperor penguins, kings of ice . First article: 55 years of vicuna conservation . Australia is home to many unique mammals because they have evolved in geographic isolation for millennia. Over 200 years ago, European colonists brought their own mammals to Australia, devastating this unique wildlife in ways that can still be seen today. One example is the rock-wallabies ( Petrogale spp. ), a group of 25 animal species and subspecies related to kangaroos. Australian scientists are monitoring rock-wallaby populations to ensure they remain safe from natural and human-caused threats. This article will describe those threats and how rock wallabies are being conserved. Rock-wallaby habitat As their name suggests, rock-wallabies are adapted to occupy specific rocky habitats, including outcrops, cliffs and caves. Since they are primarily nocturnal, these habitats provide shelter in the daytime. Rock-wallabies have modified foot pads to grip tricky surfaces and access places their predators cannot. Recent research found that for two rock-wallaby species, their abundance is associated with more complex and rocky habitats. Because their habitat type is so niche and they rarely migrate, one small disturbance could wipe out an entire rock-wallaby population. This is reflected by their protections under Australian law: five types of rock-wallaby are classified as ‘vulnerable’, six as ‘endangered’, and one as ‘critically endangered’. Thus, the complex habitat of rock-wallabies is both a blessing and a curse. Threats to rock-wallabies Rock-wallabies are vulnerable or endangered mainly because of invasive predators such as foxes, cats, and goats. After being introduced from Europe during colonisation, these predators have eaten many wallabies and scared the rest into foraging elsewhere. If predators live between two rock-wallaby populations, there will be less migration and interbreeding, reducing overall genetic health ( Figure 1 ). In addition, rock-wallabies will not forage if predators are in an area, so they have limited food sources under high pressure ( Figure 1 ). Combined with these indirect reasons, direct predation by invasive mammals is the biggest threat to rock-wallaby survival. Invasive predators are not the only threats to rock-wallaby populations. Wildfires kill the plants that wallabies rely on for food and shelter, such as rock figs. For example, one wildfire in the 2019/2020 season destroyed about 38% of brush-tailed rock-wallaby habitat. The already dwindling rock-wallaby populations may disappear if the climate crisis makes wildfires less predictable and more severe. Native herbivores like the euro and invasive herbivores like goats may also compete with rock-wallabies for food. There is evidence that euros out-compete rock-wallabies when food supplies are limited, but no evidence for goats yet. Thus, fires and competition combine with invasive predators to endanger rock-wallabies. Translocation and monitoring Monitoring existing rock-wallaby populations and creating new ones by translocation are reducing the threats of predation, fire, and competition. Brush-tailed rock-wallabies were translocated to Grampians National Park in 2008, but most animals died by 2013. Scientists thought manually handling wallabies might make them stressed and more vulnerable to predators. From 2014 onwards, non-invasive monitoring procedures like cameras and faecal DNA monitoring reduced predation and increased the survival rate of young rock-wallabies. Meanwhile, black-flanked rock-wallabies were being translocated from four different source populations to Kalbarri National Park, hoping they would interbreed and create a new genetically diverse population. The project was successful, as microsatellite genotyping found that the translocated population had more heterozygotes and more alleles per locus than the source populations ( Figure 2 ). This population is predicted to grow until at least 2028 because it is diverse enough to avoid the inbreeding mentioned earlier. The Grampians and Kalbarri translocations show the importance of careful monitoring and genetic considerations for conserving rock-wallabies. Conclusion After invasive mammalian predators have decimated rock-wallaby populations throughout Australia for over 200 years, wildfires and herbivore competition make survival even more difficult. Conservation efforts are made harder by the specific and limited habitats that rock-wallabies need. However, translocation efforts which consider genetic diversity and the stress of manual handling keep rock-wallaby populations afloat. Written by Simran Patel Related article: Wildlife corridors REFERENCES Campbell, I. & Woods, S. (2013) Wildlife of Australia . Princeton, UNITED STATES: Princeton University Press. Kleemann, S., Sandow, D., Stevens, M., Schultz, D.J., Taggart, D.A. & Croxford, A. (2022) Non-invasive monitoring and reintroduction biology of the brush-tailed rock-wallaby (Petrogale penicillata) in the Grampians National Park, Australia. Australian Journal of Zoology . 69 (2): 41–54. Available from: https://www.publish.csiro.au/zo/ZO21009 (Accessed 10th December 2024). Lavery, T.H., Eldridge, M., Legge, S., Pearson, D., Southwell, D., Woinarski, J.C.Z., Woolley, L.-A. & Lindenmayer, D. (2021) Threats to Australia’s rock-wallabies (Petrogale spp.) with key directions for effective monitoring. Biodiversity and Conservation . 30 (14): 4137–4161. Available from: https://doi.org/10.1007/s10531-021-02315-3 (Accessed 9th December 2024). Morris, S.D., Johnson, C.N. & Brook, B.W. (2020) Roughing it: terrain is crucial in identifying novel translocation sites for the vulnerable brush-tailed rock-wallaby (Petrogale pencillata). Royal Society Open Science . 7 (12): 201603. Available from: https://royalsocietypublishing.org/doi/full/10.1098/rsos.201603 (Accessed 10th December 2024). Nilsson, K., Pearson, D., Paxman, M., Desmond, A., Kennington, J., Byrne, M. & Ottewell, K. (2023) Translocations restore a population of a threatened rock-wallaby and bolster its genetic diversity. Conservation Genetics . 24 (5): 547–561. Available from: https://doi.org/10.1007/s10592-023-01520-7 (Accessed 9th December 2024). Silcock, J.L., Gynther, I.C., Horsup, A., Molyneux, J., Wattz, T.L., Fairfax, R.J., Healy, A.J., Murphy, D. & McRae, P.D. (2024) Half a century of survey data reveal population recovery but persistent threats for the Vulnerable yellow-footed rock-wallaby in Queensland, Australia. Oryx . 1–13. Available from: https://www.cambridge.org/core/journals/oryx/article/half-a-century-of-survey-data-reveal-population-recovery-but-persistent-threats-for-the-vulnerable-yellowfooted-rockwallaby-in-queensland-australia/D976E61ABE458B9FADA059372117382E (Accessed 10th December 2024). Project Gallery

Uncovering the role of IGF2BP1 in neuroblastoma and its potential as a therapeutic target Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Novel neuroblastoma driver: a potential target for therapeutics Last updated: 24/06/25, 14:16 Published: 03/07/25, 07:00 Uncovering the role of IGF2BP1 in neuroblastoma and its potential as a therapeutic target Introduction Neuroblastoma is a complicated cancer of the nervous system that primarily affects children, particularly those under the age of five. It is characterised by the development of tumours originating from neural crest cells involved in the formation of the adrenal glands and sympathetic nervous system. As the most common extracranial solid tumour in infancy and childhood, neuroblastoma represents a significant challenge in paediatric oncology due to its complex biology and variable prognosis. Recent advancements have brought hope by identifying a novel genetic driver, IGF2BP1 , implicated in the aggressive progression of the disease. The University Medicine Halle team's breakthrough in pinpointing IGF2BP1 's role is significant. It paves the way for understanding the molecular underpinnings of neuroblastoma. Additionally, it opens the door to potentially transformative targeted therapies. By elucidating the mechanisms through which IGF2BP1 drives tumour growth—specifically through its interaction with oncogenes such as MYCN —researchers are making significant progress. They are closer than ever to devising strategies that could arrest the disease's development. This progress could significantly improve patient outcomes. The importance of this discovery cannot be overblown, as it provides a crucial target for therapeutic intervention, potentially leading to the development of more effective, less toxic treatments. This is a significant step towards not only enhancing survival rates but also the quality of life for affected children worldwide. IGF2BP1: a key player in neuroblastoma and potentially other tumours The IGF2BP1 gene has emerged as a crucial element in neuroblastoma pathogenesis. It functions as an RNA-binding protein that enhances the stability and translation of mRNA transcripts. These transcripts encode oncogenic proteins, significantly impacting tumour behaviour. Oncogenes are genes that have the potential to cause cancer by promoting uncontrolled cell division and tumour growth. The activation of IGF2BP1 leads to the increased expression of several key oncogenes, including BIRC5 and MYCN. These are known to drive the growth and malignancy of neuroblastoma cells. This discovery marks a substantial leap in understanding the molecular dynamics at play within neuroblastoma cells, offering a novel avenue for targeted intervention. By stabilising and enhancing the translation of mRNA transcripts encoding these oncogenic proteins, IGF2BP1 plays a crucial role in promoting tumour growth and malignancy. Understanding this interaction provides a strategic point of intervention, potentially leading to targeted therapies that could inhibit the harmful effects of IGF2BP1 and significantly improve patient outcomes. Moreover, the IGF2BP1 role extends beyond neuroblastoma. Its expression has been detected in various other cancers, where it similarly promotes tumour growth and survival. For example, IGF2BP1 has been implicated in the progression of colorectal, breast, and lung cancers, suggesting a broader oncogenic role. This consistent pattern across different cancers underscores its potential as a universal therapeutic target. The broad impact of IGF2BP1 on multiple tumour types also highlights the potential for developing cross-cancer therapeutic strategies. By targeting IGF2BP1 , it may be possible to design treatments that are effective against multiple forms of cancer, thus maximising the impact of research and development efforts in oncology. This could lead to the creation of a new class of anticancer drugs that inhibit IGF2BP1 , offering hope to patients with various malignancies. However, targeting this gene presents challenges. IGF2BP1 is involved in beneficial processes such as normal cell growth and repair. For instance, it plays a role in stabilising mRNA during cell division, which is crucial for tissue regeneration. Inhibiting IGF2BP1 might impair these processes, leading to issues such as poor wound healing or reduced immune function. Additionally, its inhibition could potentially affect other normal cellular functions, posing a risk of unintended side effects. Thus, while targeting IGF2BP1 holds promise, understanding its role in healthy cells is essential to developing therapies that are both effective and safe. Research into IGF2BP1’s mechanisms has also revealed that it might be instrumental in initiating an “oncogene storm”. This is a rapid and intense expression of oncogenes that drives aggressive tumour growth. It also leads to resistance to conventional therapies. Conventional therapies typically refer to standard cancer treatments such as chemotherapy, radiation therapy, and surgery. For example, chemotherapy drugs like doxorubicin and cisplatin are designed to kill rapidly dividing cells, but the oncogene storm can enable tumour cells to become resistant to these drugs by enhancing their survival mechanisms. Similarly, radiation therapy aims to damage the DNA of cancer cells, but the increased expression of oncogenes can repair this damage more effectively, allowing the tumour to persist. This understanding provides a crucial insight into how cancer cells exploit molecular mechanisms to thrive and evade treatment, thereby pointing to strategic points of intervention. Current research is exploring how targeted therapies can be developed to specifically inhibit the effects of the oncogene storm, potentially overcoming resistance to these conventional treatments. This understanding provides a crucial insight into how cancer cells exploit molecular mechanisms to thrive and evade treatment, thereby pointing to strategic points of intervention. MYCN’s role in neuroblastoma: a pivotal transcriptional driver MYCN is a member of the MYC family of transcription factors, which play critical roles in cell cycle progression, apoptosis, and cellular transformation. In neuroblastoma, MYCN is particularly notorious for its strong association with high-risk disease and poor clinical outcomes, making it a main point of cancer research. High-risk disease in neuroblastoma is characterised by factors such as advanced stage at diagnosis, unfavourable histology, and the presence of MYCN amplification. For example, Stage 4 neuroblastoma, where the cancer has spread to distant lymph nodes, bone, bone marrow, liver, skin, or other organs, is considered high-risk. Poor clinical outcomes in these cases often include a lower survival rate and a higher likelihood of relapse after treatment. Studies have shown that children with MYCN -amplified neuroblastoma have a significantly lower 5-year survival rate compared to those without MYCN amplification. This is because MYCN amplification drives rapid tumour growth and metastasis, making the cancer more aggressive and difficult to treat. Additionally, these patients often exhibit resistance to conventional therapies such as chemotherapy and radiation, which further complicates treatment and negatively impacts prognosis. Specific examples of poor clinical outcomes include frequent relapses and the development of resistance to multiple lines of therapy. Despite intensive treatment regimens, including high-dose chemotherapy followed by stem cell transplant and radiation therapy, the overall survival rate for high-risk neuroblastoma remains below 50%. This bare reality underscores the critical need for novel therapeutic strategies that can effectively target MYCN and improve outcomes for patients with high-risk neuroblastoma. In general, MYCN amplifies in approximately 20% to 25% of neuroblastoma cases, leading to a dramatic increase in its protein expression. This overexpression is a known marker for aggressive disease and has been linked to rapid tumour progression and resistance to standard therapies. Standard therapies for neuroblastoma typically include a combination of surgery, chemotherapy, and radiation therapy. For instance, chemotherapy drugs such as cyclophosphamide and vincristine are commonly used to shrink tumours before surgical removal. However, the overexpression of MYCN can enhance the tumour’s ability to repair DNA damage caused by these treatments, making them less effective. Radiation therapy, which uses high-energy particles to destroy cancer cells, also becomes less effective as MYCN overexpression promotes survival pathways within the cells. The interaction between MYCN and IGF2BP1 creates a formidable axis that drives the malignant characteristics of neuroblastoma cells. Functionally, MYCN amplifies the effects of IGF2BP1 by synergising its activity. This synergy is evident in their mutual enhancement of oncogenic signalling pathways. MYCN enhances the transcription of numerous genes involved in cellular proliferation and survival. While IGF2BP1 stabilises the mRNAs of these genes, ensuring their sustained expression and activity within the cell. This interaction not only accelerates tumour growth but also contributes to the genomic instability that is characteristic of high-risk neuroblastoma. Besides, the role of MYCN extends beyond merely amplifying gene expression. It fundamentally alters the cellular landscape by modulating the expression of genes involved in metabolism, differentiation, and angiogenesis, thus shaping the tumour microenvironment to favour cancer growth and metastasis. Recent studies have also uncovered MYCN ’s role in repressing the transcription of genes involved in cellular differentiation, thereby maintaining the cells in a more primitive, stem-like state that is conducive to cancer progression. The discovery of the “oncogene storm”, a phenomenon triggered by the cooperative action of MYCN and IGF2BP1 , highlights the critical need for targeted therapeutic strategies that can disrupt this deleterious synergy. By focusing on this interaction, researchers aim to develop novel treatments that can more effectively curb the aggressive nature of MYCN -amplified neuroblastoma. The potential for therapeutic intervention The discovery of the IGF2BP1 and MYCN interaction not only deepens our understanding of neuroblastoma pathogenesis but also marks a significant step towards developing targeted therapeutic interventions. The small molecule BTYNB , which disrupts this interaction, has shown promising results in preclinical studies. By inhibiting the oncogene-enhancing effect of IGF2BP1 on MYCN , BTYNB effectively reduces tumour growth and could potentially improve the efficacy of existing treatment protocols. Current research is exploring the application of BTYNB in combination with other therapeutic agents. Combining BTYNB with existing chemotherapy drugs or novel targeted therapies may enhance treatment efficacy and prevent the onset of resistance. This combinatorial approach could be particularly effective in high-risk neuroblastoma cases, where conventional treatments often fall short. Additionally, understanding the pharmacodynamics and optimising the dosing schedule of BTYNB are critical areas of ongoing research to maximise its therapeutic potential and minimise side effects. This includes studying how the drug is absorbed, distributed, metabolised, and excreted in the body to ensure optimal efficacy. For instance, researchers are investigating the timing and dosage that maximise tumour reduction while minimising toxicity. Examples include adjusting the frequency of administration to maintain therapeutic levels and combining BTYNB with other agents to enhance its effects. These efforts aim to maximise its therapeutic potential and minimise side effects. Furthermore, the ability of BTYNB to impair tumour growth without the severe side effects associated with conventional chemotherapy presents an opportunity to reduce the treatment burden on patients. This aspect is crucial, especially in paediatric oncology, where the long-term health of young patients is a significant concern. Future therapeutic strategies could see BTYNB becoming part of a first-line treatment for neuroblastoma, either as a standalone therapy or in combination with other treatments. Future directions The ground-breaking discovery of the IGF2BP1 - MYCN interaction in neuroblastoma provides solid initial results with BTYNB , and the identification of IGF2BP1 as a key driver in neuroblastoma opens several avenues for future research. One critical area involves further elucidation of the molecular mechanisms underlying IGF2BP1 ’s influence on neuroblastoma progression. Continued research is necessary to dissect the finer details of the molecular pathways modulated by IGF2BP1 and MYCN . This includes understanding the downstream effects of their interaction and identifying other molecular players involved in the signalling cascade. Insights from such studies could reveal novel personalised therapeutic targets and help in designing drugs that can more precisely disrupt these pathways. Additionally, given the role of IGF2BP1 in various cancers, research should also explore its potential as a universal cancer target. Comparative studies across different cancer types could identify shared patterns of IGF2BP1 activity, offering opportunities to develop broad-spectrum anticancer strategies. Developing targeted delivery mechanisms that can direct BTYNB or other similar drugs specifically to neuroblastoma cells could significantly enhance therapeutic outcomes and reduce side effects. Research into nanoparticle-based delivery systems or conjugated molecules that seek out cancer-specific markers could be particularly fruitful. Additionally, investigating other compounds that can target IGF2BP1 or MYCN could provide alternative therapeutic options or complementary strategies to overcome resistance. Strategic integration of new therapies into existing treatment protocols needs careful planning. This includes determining the optimal sequencing of therapies and identifying which combinations are most effective for various subtypes of neuroblastoma based on genetic characteristics. Clinical trials are essential to transitioning laboratory findings to clinical applications. Designing and implementing rigorous clinical trials to test the efficacy and safety of BTYNB , both as a monotherapy and in combination with other therapies, is crucial. These trials should incorporate robust biomarker studies to tailor therapies based on genetic profiles and monitor patient responses more effectively. Lastly, addressing the challenge of drug delivery remains paramount. Developing drug delivery systems that can effectively target tumour sites with minimal off-target effects could improve the therapeutic index of treatments like BTYNB . Research in this area will not only benefit neuroblastoma patients but also advance the field of targeted cancer therapy in general. Importantly, given the young age of neuroblastoma patients, it is imperative to consider long-term outcomes and quality of life in therapeutic development. Efforts must be made to ensure that new treatments are not only effective but also minimise the long-term health impacts often associated with aggressive cancer therapies. Conclusion The identification of IGF2BP1 as a pivotal driver in the pathogenesis of neuroblastoma, particularly in concert with MYCN , marks a significant milestone in paediatric oncology. This discovery not only enhances our molecular understanding of one of the most challenging childhood cancers but also sets the stage for the development of targeted therapeutic strategies that could revolutionise treatment paradigms. The potential of BTYNB , a small molecule inhibitor that disrupts the IGF2BP1 - MYCN interaction, underscores the power of targeted therapy. In preclinical models, BTYNB has demonstrated a promising ability to inhibit tumour growth effectively and with fewer side effects compared to traditional chemotherapy. Such advancements herald a new era in treatment where therapy is not only about fighting the disease but also preserving the quality of life for the youngest patients. However, the journey from laboratory to clinic is filled with challenges that require innovative solutions and collaborative efforts. These challenges include ensuring the safety and efficacy of new treatments, overcoming drug resistance, and achieving precise delivery to tumour sites. The future of neuroblastoma treatment lies in the ability to refine these emerging therapies through rigorous research, optimise their delivery, and integrate them seamlessly into existing treatment protocols. Additionally, the exploration of IGF2BP1 's role across various cancer types may provide insights that transcend paediatric oncology, offering new hope for comprehensive cancer treatment strategies. As the research advances, it will be crucial to maintain a multidisciplinary approach, combining the expertise of molecular biologists, clinical researchers, and pharmacologists to ensure that these new discoveries translate into safe and effective treatments. The engagement of global health communities in these efforts will be essential to address the diverse and complex nature of cancer treatment across different populations. All in all, the path forward is marked by significant potential and profound responsibility—to continue the search for knowledge and to translate that knowledge into therapies that not only extend life but also enhance the lived experiences of patients during and after treatment. With continued dedication and innovation, the future for children battling neuroblastoma looks increasingly hopeful. Written by Sara Maria Majernikova Related articles: Cancer on the move (metastasis) REFERENCES Hagemann, S., Misiak, D., Bell, J. L., Fuchs, T., Lederer, M. I., Bley, N., Hämmerle, M., Ghazy, E., Sippl, W., Schulte, J. H., & Hüttelmaier, S. (2023). IGF2BP1 induces neuroblastoma via a druggable feedforward loop with MYCN promoting 17q oncogene expression. Molecular cancer , 22 (1), 88. https://doi.org/10.1186/s12943-023-01792-0 Liu, Y., Guo, Q., Yang, H., Zhang, X. W., Feng, N., Wang, J. K., Liu, T. T., Zeng, K. W., & Tu, P. F. (2022). Allosteric Regulation of IGF2BP1 as a Novel Strategy for the Activation of Tumor Immune Microenvironment. ACS central science , 8 (8), 1102–1115. https://doi.org/10.1021/acscentsci.2c00107 Project Gallery

Cultural beliefs, stigma, family values and more, inhibit open discussion of mental health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Addressing mental health within the South Asian community Last updated: 27/11/25, 15:14 Published: 22/05/25, 07:00 Cultural beliefs, stigma, family values and more, inhibit open discussion of mental health Mental health is a critical aspect of human life, yet it remains a deeply taboo subject within the South Asian community. Despite the growing awareness in mainstream discourse, many South Asians—especially those living in diasporic communities such as the UK, the US, and Canada—continue to face significant barriers when it comes to recognising, understanding, and seeking help for mental health concerns. But why does this silence continue? The answer lies in a combination of cultural beliefs, stigma, family values, societal expectations, and a general lack of education, especially among the older generations. Unlike Western cultures, which tend to emphasise individualism, South Asian societies often focus on collectivism, where the success and well-being of the family take precedence over the individual. This cultural foundation has both strengths and challenges. While it preaches community and support, it also discourages expressions of emotional vulnerability, especially when that vulnerability may be perceived as bringing shame or dishonour to the family. Mental health is often viewed as a personal weakness, a spiritual failing, or something that reflects poorly on one’s upbringing or family reputation. A survey conducted by the NHS in the UK revealed that 35% of South Asian youth aged 18–24 reported experiencing some form of mental health issue, compared to 30% of White British youth. While these figures suggest a slightly higher incidence, what is more alarming is the disparity in access to care and treatment. Many South Asians are less likely to seek help due to fears of being perceived as 'crazy' or weak. In some cases, mental health symptoms are dismissed as temporary mood swings, spiritual crises, or simply a lack of willpower. A study published by the Mental Health Foundation (2020) found that only 32% of South Asians surveyed had a functional understanding of mental health, compared to 60% of the general UK population. This suggests that stigma is caused by a lack of knowledge, which prevents early intervention and exacerbates untreated conditions. Among those who recognise they have a problem, there is often a reluctance to seek professional help, particularly from psychologists or psychiatrists. Instead, some may turn to spiritual leaders or rely solely on familial support, both of which, while culturally significant, may not always offer the necessary therapeutic intervention. One of the major mental health concerns within the South Asian community is depression and anxiety, and these conditions often go undiagnosed. Research from the Centre for Mental Health has indicated that South Asian individuals are more likely to report symptoms of depression and anxiety than their White counterparts, but are less likely to receive treatment. According to a 2022 study by Public Health England, South Asian women are 1.5 times more likely to suffer from common mental health disorders, such as anxiety and depression, but only 13% accessed mental health services compared to 25% of White British women. Many culturally specific factors contribute to higher rates of anxiety and depression in South Asian communities. These include intergenerational trauma, immigration stress, identity conflict, and pressures related to marriage, family reputation, and academic or career success. Young South Asians often find themselves navigating between traditional family expectations and Western societal norms, leading to identity struggles that can trigger chronic stress and anxiety. Additionally, gender roles in South Asian cultures often impose strict expectations on behaviour. Women may be discouraged from voicing emotional distress, as they are expected to be nurturing and self-sacrificing. Men, on the other hand, are often pressured to appear strong and unemotional, which leads to a culture where expressing vulnerability is equated with failure. These rigid expectations prevent both genders from openly discussing their struggles or seeking help. Barriers to accessing mental health services are not only cultural but also structural. Many South Asians, particularly first-generation immigrants, may face language barriers when communicating with healthcare providers. There is also a lack of culturally competent therapists who understand the nuances of South Asian traditions, values, and family structures. Without representation or relatability, individuals may feel misunderstood or alienated by the mental healthcare system. Despite these challenges, there is hope. The rise of South Asian mental health advocates, community-based initiatives, and culturally tailored therapy programs is slowly helping to dismantle stigma. Social media has also played a vital role in bringing these conversations to the forefront, especially among Gen Z and Millennials. Many people are now speaking out and sharing their stories and experiences, which helps shift the narrative within the South Asian Community. We can help break the stigma surrounding mental health in the South Asian community by raising awareness, educating others, and normalising conversations around emotional wellbeing. It starts at the grassroots level: in homes, schools, religious institutions, and workplaces. Encouraging open dialogue and fostering environments where individuals feel safe to share their experiences without judgment is key. More importantly, we must validate the struggles of those suffering from mental health issues—telling them that it is okay to not be okay, and that seeking help is a sign of strength, not weakness. Furthermore, the government and health services can do more! They should invest in culturally sensitive mental health resources, including multilingual therapy options and outreach programs tailored specifically for South Asian populations. In conclusion, addressing mental health within the South Asian community requires a collective effort to challenge outdated norms, educate people across all age groups, and improve access to inclusive and empathetic mental healthcare. Depression, anxiety, and other mental illnesses are not signs of weakness; they are real, treatable conditions that deserve compassion and support. Only by acknowledging this and working together can we begin to transform the narrative and create a healthier, more open future for the South Asian community, letting the future generation have a safe and open space to talk and get help for their mental health! Written by Rajeevan Sinnathurai ------- Scientia News thanks Rajeevan of Open Talk, for this enlightening piece on mental health in the South Asian Community. Connect with Open Talk on Instagram and TikTok . ------- Related articles: Mental health awareness / Imposter syndrome / Anxiety / South Asian epigenetics / Global health injustices- Kashmir , Bangladesh , Sri Lankan Tamils REFERENCES NHS Digital. (2021). Mental Health of Children and Young People in England . Mental Health Foundation. (2020). Mental Health in the South Asian Community . Centre for Mental Health. (2022). Race and Mental Health Inequalities . Public Health England. (2022). Mental Health Services Use by Ethnic Groups in the UK . Project Gallery