In some cases, the exact cause of vertigo remains unidentified, highlighting the complexity of diagnosis Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Vertigo Last updated: 25/08/26, 13:59 Published: 03/07/25, 08:00 In some cases, the exact cause of vertigo remains unidentified, highlighting the complexity of diagnosis Vertigo is a symptom characterised by the sensation of spinning or movement, affecting either the individual or their surroundings. Unlike dizziness, which involves a floating sensation, or imbalance, which reflects unsteadiness, vertigo conveys a distinct sense of motion. While it is not a condition in itself, vertigo often indicates an underlying issue and can range from mild to debilitating, significantly impairing balance and daily activities. Physiology of vertigo Physiologically, vertigo is primarily linked to the inner ear and the vestibular system, which is responsible for maintaining balance and spatial orientation. The vestibular apparatus consists of semicircular canals and otolith organs, which detect angular and linear movements, respectively. Dysfunction in these structures, or their neural pathways to the brainstem and cerebellum, can disrupt normal sensory input, causing vertigo. Symptoms ( Figure 1 ) may include a spinning sensation, nausea, vomiting, nystagmus (involuntary eye movements), sweating, and difficulty with balance. Triggers vary widely and may include head movements, changes in position, or even psychological stress. The underlying causes can be peripheral, such as inner ear disorders, or central, involving the brain or central nervous system. Causes and prevalence Vertigo is particularly common among middle-aged and older adults, where it presents a considerable risk of falls and associated injuries. This demographic is especially vulnerable due to age-related changes in the vestibular system, such as a decline in vestibular hair cells and neurons, as well as alterations in central pathways. Vestibular disorders are among the most frequent causes of vertigo episodes in the elderly, often contributing to a cycle of psychological distress and physical limitation. Anxiety and depressive syndromes further exacerbate this cycle by increasing fear of attacks and falls, ultimately limiting daily activities and lowering perceived quality of life. Benign Paroxysmal Positional Vertigo (BPPV) is the most common cause of vertigo and is featured in multiple studies within the literature ( Figure 2 ). BPPV is typically triggered by changes in head position, leading to brief episodes of intense vertigo. Despite its prevalence, management can be challenging due to the nonspecific nature of symptoms and the diverse underlying causes. Recent research has also identified a strong association between vitamin D deficiency and recurrent BPPV, as vitamin D plays an important role in calcium metabolism and the maintenance of the calcium crystals (otoconia) within the inner ear. In some patients, correcting vitamin D deficiency may help reduce the risk of recurrence. Other common vestibular disorders include labyrinthitis and vestibular neuritis, which are usually caused by viral infections such as the common cold or influenza. These conditions result in inflammation of the inner ear or vestibular nerve and can cause sudden, severe vertigo lasting several days, often accompanied by nausea, vomiting, and imbalance. Vestibular migraine is another increasingly recognised cause of recurrent vertigo and may occur with or without a typical migraine headache, making diagnosis challenging. The COVID-19 pandemic has also highlighted Long COVID (Post-COVID Condition) as an emerging cause of persistent dizziness and vertigo. Some individuals continue to experience balance disturbances and vestibular symptoms for weeks or months following their initial infection, contributing to ongoing functional impairment. Polypharmacy, or the use of multiple medications, has also emerged as a significant factor in vertigo among older adults. Prescriptions involving several drugs, particularly antihypertensives and sedative hypnotics, have been linked to an increased likelihood of vertigo. Careful assessment of medication interactions and side effects during medical consultations is therefore essential. Metabolic disorders, such as diabetes and hypoglycaemia, also contribute to vertigo in some individuals. Although the majority of vertigo cases originate from disorders of the inner ear, neurological conditions should also be considered. Stroke and other central nervous system disorders account for an estimated 10–20% of vertigo presentations in acute care settings and are more likely when vertigo is accompanied by symptoms such as slurred speech, facial weakness, numbness, double vision, severe headache, or difficulty walking. These features require urgent medical assessment to exclude a potentially life-threatening cause. However, in a proportion of cases, the exact cause of vertigo remains unidentified, highlighting the complexity of diagnosis and the importance of a comprehensive clinical assessment. Conclusion As one of the most common and disabling symptoms in the elderly, vertigo requires comprehensive and individualised care. Understanding its underlying physiological mechanisms, as well as recognising the multifactorial influences such as medication use, psychological health, and metabolic disorders, is essential for effective management. By adopting an integrated approach that prioritises accurate diagnosis and targeted interventions, clinicians can improve both symptom control and overall quality of life for individuals affected by vertigo. Further research is needed to enhance treatment strategies and address the remaining gaps in knowledge. Written by Maria Z Kahloon Project Gallery

The current conflict has caused unfathomable mental distress and health problems for the Kashmiri people Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Health gaps in conflict-affected Kashmir Last updated: 18/09/25, 09:41 Published: 17/07/25, 08:00 The current conflict has caused unfathomable mental distress and health problems for the Kashmiri people This is article no. 5 in a series about global health injustices. Previous article: Syria and Lebanon ’s diverging yet connected struggles . Next article: Health inequalities in Bangladesh . Introduction Welcome to the fifth article of the Global Health Injustices Series. The previous article was a collaborative endeavour focused on the populations in Syria and Lebanon. Now, I will focus on the people living in Kashmir, who are currently experiencing a lot of health and wellbeing challenges, primarily attributed to conflict. For example, on top of the enduring conflict in Kashmir, the COVID-19 pandemic had worsened the mental health of the Kashmiri population, where 1.8 million adults were living with any type of mental distress. Despite these concerns, the Kashmiri people have not had their voices heard as clearly in mainstream discourse compared to other vulnerable populations discussed in previous articles. Kashmir: a rich history to current conflict Kashmir (also known as Jammu & Kashmir) is a region within the Northern Indian subcontinent, bordered mainly by Pakistan and China. Kashmir is a disputed territory between the militaries of India and Pakistan since the Indian subcontinent was divided up by the British Empire in 1947. Even before that, conflicts were driven by issues with local governments and tensions between cultural and ethnic groups within the region. These issues, among others, have contributed to the instability and health challenges encountered by the Kashmiri people. In recent years, tensions and violence have accelerated, particularly in 2024, due to the Indian government wanting to maintain control of the Kashmiri region. This has led to vast protests and friction between civilians and armed forces. In turn, this has weakened ties within the region, particularly between India and neighbouring nations. Another overlooked impact (which I will be discussing further) of this current conflict is on Kashmiri women, who encounter certain challenges, which include loss of family members, displacement and Gender-Based Violence. Considering this background of Kashmir is crucial because it will help with understanding the current geopolitical climate and how it detrimentally affects the health of the Kashmiri people. Geopolitics and health in Kashmir Similar to the populations discussed in previous articles, the Kashmiri people are encountering a lot of mental distress attributed to the ongoing conflict. One study from 2009 found that the prevalence of depression was 55.72%. Meanwhile, another study from 2017 uncovered that approximately 45% of adults experienced mental distress, with specific rates of 41% for depression, 26% for anxiety, and 19% for post-traumatic stress disorder (PTSD). This difference presumably came from wider geopolitical factors, as measuring mental health is challenging during conflict. As such, the healthcare system in Kashmir needs urgent improvement to better support mental health. Even though it does better in some areas compared to the national average, the demand for services, especially in conflict-affected areas, is overwhelming. There are not enough mental health professionals, and many healthcare providers lack the training to handle trauma-related issues properly. Investing in training, community mental health initiatives, and integrating mental health services with regular healthcare could help improve the overall mental health of the Kashmiri people. Focusing on mental health just as much as physical health to build resilience in Kashmir is essential. As for the health infrastructure in Kashmir, noted in one review, they have 4433 government health institutions and a doctor-patient ratio of 1:1880, which is lower than the World Health Organisation (WHO) recommendation of 1:1000, yet higher than the national level of 1:2000. Moreover, the state of Kashmir was shown to have better health indices compared to the national average, including life expectancy, infant mortality rate, and crude birth and death rates. Despite these improvements, challenges persist, such as the inadequate health infrastructure and a shortage of financial resources and technical staff, despite relatively stable trends ( Table 1 ). In one study, the authors noted that among the Schedule tribes in Kashmir, they encounter significant health challenges attributed to illiteracy, poverty, and inadequate healthcare facilities and infrastructure, leading to increased non-communicable diseases (NCDs). There is a high prevalence of poor nutrition and undernutrition, which contributes to the susceptibility of these populations to NCDs (7). Moreover, a lack of access to clean water and sanitation worsens health issues, which increases their risk of infectious diseases. Social taboos and beliefs hinder healthcare service utilisation among the population, which impacts health outcomes and even awareness of NCDs ( Figure 1 ). Focusing on violence exposure in Kashmir, another study among households found that respondents documented high levels of violence, which include: exposure to crossfire (85.7%), round-up raids (82.7%), witnessing torture (66.9%), experiences of rape (13.3%) and forced labor (33.7%). What this study also found was that males noted more violent confrontations and had higher odds of experiencing different forms of maltreatment compared to females. Given that this study was conducted in 2008, these figures are likely to be either higher or lower now, depending on the magnitude of violence and warfare. Nonetheless, the high frequency of violence has led to substantial health issues, specifically mental health problems among the affected Kashmiri population. A severely overlooked impact of conflict in Kashmir is on the women, who encounter specific tragedies, including loss of family members and displacement. Moreover, the use of rape as a weapon in conflict stresses the convergence of gender and political power, particularly in Kashmir. Unfortunately, there have been some researchers who usually depict Kashmiri women as solely victims, which can undermine their autonomy and political involvement. Therefore, addressing the plight of Kashmiri women by allowing them to discuss their experiences openly and actively involving them in key decisions regarding Kashmir can be a vital stepping stone towards supporting their health and well-being. To truly understand all of the various health challenges illustrated above impacting the Kashmiri population, it is vital to cite the various geopolitical factors I discussed in previous articles on Yemen, Sudan and Palestine. The most notable factor is the continuous international weapons/ arms trade, which I firmly believe must be thwarted because of how much damage it has caused, particularly through the sale of bombs and other explosives used to target the most vulnerable populations. However, stopping this trade requires actual political will and legislation, which is unlikely to happen anytime soon because our leaders make a lot of profit from selling weapons. NGOs: their role in supporting Kashmir International non-governmental organisations (INGOs), notably Aakar Patel, chair of board at Amnesty International India, shared this statement in 2024 regarding Kashmir: The Indian authorities are using arbitrary restrictions and punitive actions to create a climate of fear in Jammu and Kashmir. Anyone daring to speak out – whether to criticize the government or to stand up for human rights – faces a clampdown on their rights to freedom of expression and association and cannot move freely within and outside the country. Amnesty International also shared testimonies from a few Kashmiri people: I feel a deep responsibility to be the voice of my people, who are currently voiceless. There are no stories coming out of Kashmir anymore. - Masrat Zahra, an award-winning Kashmiri photojournalist. My freedom of movement is a right enshrined in the Indian Constitution, but I had to really struggle to exercise this right. - Iltija Mufti, daughter and media advisor to ex-chief minister of Jammu & Kashmir. To address the complex health and social issues previously discussed, international organisations and local communities need to come together for solutions. Programs focusing on building mental health support, improving healthcare availability, and creating safe spaces for women and young people can make a difference. The Kashmiri people need to have their voices heard in discussions about their health and wellbeing. Otherwise, their challenges will continue to affect their lives. Conclusion Overall, the health and well-being issues in Kashmir are closely linked to the long-standing conflict and warfare. Although this region has a rich cultural history and shows a lot of resilience, the current conflict has caused unfathomable mental distress and health problems for the Kashmiri people. The rise in mental health issues and the inadequate healthcare infrastructure illustrate that reforms are urgently needed. There is a real shortage of support for mental health, particularly when dealing with the trauma from ongoing violence. Moreover, marginalised groups face tremendous health challenges because of various factors ranging from poverty to a lack of education to limited access to basic needs. Living in violence and conflict not only affects physical health, but also leads to ongoing psychological trauma that is often ignored. Tackling these health inequalities and inequities requires a comprehensive approach incorporating mental health care into the standard healthcare system, improving access to clean water and food, and building communities. Listening to the Kashmiri people and focusing on their health needs is key to achieving peace and better living standards in the region. Therefore, national and international players must recognise these issues and take real action to ensure they receive the support they need and deserve. Only with continued efforts can we expect a healthier future for Kashmir. The following article in the Global Health Injustices series will focus on Bangladesh and the plight of the Rohingya population, which will also be a collaborative endeavour. Written by Sam Jarada Related articles: Impacts of global warming on dengue fever / Understanding health through different stances / South Asian famine / South Asian mental health REFERENCES Sheikh Shoib, Arafat SMY. Mental health in Kashmir: conflict to COVID-19. Public Health. 2020 Sep 1;187:65–6. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC7484691/ Center for Preventive Action. Conflict Between India and Pakistan. Global Conflict Tracker. 2015. Available from: https://www.cfr.org/global-conflict-tracker/conflict/conflict-between-india-and-pakistan Zeeshan S, Hanife Aliefendioğlu. Kashmiri women in conflict: a feminist perspective. Humanities and Social Sciences Communications. 2024 Feb 12;11(1). Available from: https://www.nature.com/articles/s41599-024-02742-x Amin S, Khan A. Life in conflict: Characteristics of Depression in Kashmir. International Journal of Health Sciences. 2009 Jul;3(2):213. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC3068807/ Housen T, Lenglet A, Ariti C, Shah S, Shah H, Ara S, et al. Prevalence of anxiety, depression and post-traumatic stress disorder in the Kashmir Valley. BMJ Global Health. 2017 Oct;2(4):e000419. Available from: https://gh.bmj.com/content/2/4/e000419 Mir A, Bhat S. Health Status and Access to Health Care Services in Jammu and Kashmir State. Asian Review of Social Sciences [Internet]. 2018;7(3):52–7. Available from: https://www.trp.org.in/wp-content/uploads/2018/11/ARSS-Vol.7-No.3-October-December-2018-pp.52-57.pdf Habib A, Iqbal A, Rafiq H, Shah A, Amin S, Suheena, et al. Trends in the Magnitude of NCDs among Schedule Tribe Population of Kashmir with Special Reference to Health and Nutritional [Internet]. Journal of Community Medicine & Public Health. Gavin Publishers; 2023 [cited 2025 May 5]. Available from: https://www.gavinpublishers.com/article/view/trends-in-the-magnitude-of-ncds-among-schedule-tribe-population-of-kashmir-with-special-reference-to-health-and-nutritional Jong K de, Ford N, van, Kamalini Lokuge, Fromm S, Galen R van, et al. Conflict in the Indian Kashmir Valley I: exposure to violence. Conflict and Health [Internet]. 2008 Oct 14 [cited 2025 May 5];2(1). Available from: https://conflictandhealth.biomedcentral.com/articles/10.1186/1752-1505-2-10 Authorities must end repression of dissent in Jammu and Kashmir [Internet]. Amnesty International. 2024 [cited 2025 Jun 11]. Available from: https://www.amnesty.org/en/latest/news/2024/09/india-authorities-must-end-repression-of-dissent-in-jammu-and-kashmir/ Project Gallery

Exploring neuroplasticity after brain injury Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can we really ‘rewire’ our brain? Last updated: 06/05/26, 21:11 Published: 07/05/26, 08:00 Exploring neuroplasticity after brain injury Can the brain really rebuild what has been lost after a brain injury? This idea derives from neuroplasticity – the nervous system’s capacity to change and adapt, reorganising its connections and overall structure as a result of an experience. In other words, the brain strengthens, weakens, and forms new neural connections over time. In psychology, neuroplasticity is crucial for understanding learning, as repeated behaviours and thoughts can strengthen neural pathways, resulting in increased automatic responses. Neuroplasticity plays a large role in recovery following a brain injury. Joy & Carmichael (2020) found that after a stroke, the brain becomes temporarily plastic, during which new axons and synapses may form, functions can be reassigned to undamaged brain regions, and the brain becomes flexible to training, allowing for recovery. A key takeaway is that after a stroke, the brain not only repairs itself but also enters a temporary state of reorganisation and recovery. Repeated practice during rehabilitation supports the formation of new pathways, helping lost skills to be regained. This is a core psychological principle: learning requires repetition, and without it, new neural pathways will not be produced or maintained. This reorganisation is driven by cellular processes that modify neural connections. Specialised immune cells, known as microglia, reshape connections between neurons and assist in incorporating new cells into preexisting networks, as demonstrated by Sandvig et al. (2018). This emphasises that recovery is not solely biological but also behavioural, as the way one interacts with their environment influences the way the brain reorganises itself. For example, when an individual performs a behaviour, such as moving their leg in rehab, neural pathways for that certain behaviour are activated frequently. Here, microglia respond to this activity by strengthening frequently used connections and removing unused ones, a process known as “use it or lose it”, in relation to neural pathways. So, can we really ‘rewire’ our brains? Yes, but to an extent! Neuroplasticity illustrates that the brain is capable of change, through reinforced behaviour and experience, though it should be noted that this process rarely results in complete normalcy. From a psychological perspective, neuroplasticity highlights that recovery is about how behaviour, experience, and learning intertwine to allow the brain’s ability to adapt. Written by Shreya Dhaliwal Related articles: Brain injury / Synaptic plasticity REFERENCES Cleveland Clinic. (2023, December 13). Brainwork: The Power of Neuroplasticity . https://health.clevelandclinic.org/neuroplasticity . Joy , M. T., & Carmichael, S. T. (2020). Encouraging an excitable brain state: mechanisms of brain repair in stroke. Nature Reviews Neuroscience, 22 (1), 38–53. https://doi.org/10.1038/s41583-020-00396-7 . Kreber, L. (2025). Neuroplasticity . Centre for Neuro Skills. https://www.neuroskills.com/neuroplasticity/ . Mateos-Aparicio, P., & Rodríguez-Moreno, A. (2019). The impact of studying brain plasticity. Frontiers in Cellular Neuroscience, 13 . https://doi.org/10.3389/fncel.2019.00066 . Sandvig, I., Augestad, I. L., Håberg, A. K., & Sandvig, A. (2018). Neuroplasticity in stroke recovery. The role of microglia in engaging and modifying synapses and networks. European Journal of Neuroscience, 47 (12), 1414–1428. https://doi.org/10.1111/ejn.13959 Project Gallery

It's extremely pronounced in a technical environment Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link You're not a fraud: battling imposter syndrome in STEM Last updated: 22/05/25, 11:01 Published: 17/04/25, 08:00 It's extremely pronounced in a technical environment Background If you work in STEM or take even a keen interest in the field, it’s highly likely you’d have heard of and possibly experienced the term 'imposter syndrome'. Despite the glamorised success stories and carefully curated achievements we see in professional circles and on social media, let’s take a realistic step back - people struggle no matter how qualified they are. It’s okay to admit that, and it’s time we remove the stigma of this common experience. Coming into the Scientist Training Programme, I felt a sense of excitement and pride in my achievement of having even managed to get a place on the programme. As I settled in, this quickly turned into something else – fear, anxiety, worry. Feelings that I may not be good enough or I’m not where I belong. I seemed like the only one in my department without a postgraduate qualification. I began feeling out of place. It was only until I was able to put a label on this feeling – imposter syndrome, that I could take active steps to fix it. So, what is imposter syndrome? Put simply, it's the persistent feeling of self-doubt and inadequacy despite evident success. It makes you question whether you truly deserve your accomplishments, fearing that at any moment, someone will expose you as a fraud. This is extremely pronounced in a technical environment where your success is largely measured by your ability to tackle complex problems. Understanding its purpose While frustrating, imposter syndrome stems from a mechanism designed to keep us grounded and striving for growth. As social beings, we evolved to be highly attuned to hierarchies and belonging, and self-doubt may have once served as a protective mechanism, preventing reckless decisions. However, in today’s world, particularly in STEM fields, this innate caution can turn into chronic self-evaluation. The role of social media Imposter syndrome can be exacerbated through the often-unrealistic lens of social media. As I scroll through various social media platforms, I encounter countless posts showcasing often unrealistically flawless careers. Despite what you see in those 'day in the life' posts, not every STEM professional wakes up at 4am and has a cold shower. Rarely do we see the setbacks, rejections, or moments of self-doubt behind those polished posts, yet they exist for everyone. The distortion of what we see online is undoubtably a catalyst for imposter syndrome, but we can take a sensible step back and look at things through a realistic lens. Comparison truly can be the thief of joy if you let it. Coping strategies The good news is, it’s not all doom and gloom and there are strategies we can employ to handle our mischievous minds. As STEM professionals, sometimes we become isolated in our work, deeply ingrained in fixing a problem and not realising there are countless others to share your thoughts and feelings with. This is something I pushed myself to do and as I reached out to the wider community of trainee scientists, I quickly realised that I wasn’t alone. Almost everyone I had spoken to had shared a similar sentiment of having experienced imposter syndrome to some extent. It is important to remember that imposter syndrome is something that has been a universal experience for a very long time. It is certainly not a feeling that is exclusive to those in the early stages of their career as I surprisingly found out having networked with senior figures in the STEM community. My supervisor – a consultant clinical scientist with over 40 years of experience still experiences imposter syndrome as he tackles new challenges in the ever-evolving world of science. I have found that keeping a journal has been incredibly beneficial in logging my achievements -whether personal or career-related. Having a record of successes, no matter how small, serves as a tangible reminder that progress is being made, even when self-doubt tries to convince me otherwise. But the most effective tool I’ve discovered is something I’m still learning myself - self-compassion instead of self-criticism. It’s easy to be too hard on yourself, especially in STEM, where learning new things daily is the norm. The pressure to always have the right answers can make mistakes feel like failures rather than part of the learning process. But the reality is that growth comes from pushing through discomfort, not from perfection. Learning to extend yourself the same kindness you would offer a friend can make a world of difference in battling imposter syndrome. Reframing its meaning If you have experienced imposter syndrome I do have some good news for you – you’re pushing yourself out of your comfort zone in some way and challenging yourself. That is something to be proud of and its important to realise that experiencing imposter syndrome can sometimes simply be a mandatory byproduct of self-growth. You are exactly where you need to be. Even the greatest of minds can experience imposter syndrome. Albert Einstein himself once remarked: The exaggerated esteem in which my lifework is held makes me very ill at ease. I feel compelled to think of myself as an involuntary swindler. So, remember, you’re not alone in this struggle. When to seek help While imposter syndrome is something that a large majority of people experience, you should know when to seek help. If it manifests into something much more than occasional self-doubt, there is no shame in reaching out for help. Speaking to trusted friends or family about how you’re feeling is crucial to keep your mind in the right place. A qualified therapist will be well equipped to help you deal with imposter syndrome and keep you grounded. There are a wealth of online resources that can be used to help you; such as articles, self-help guides, and professional development communities – including the team here at Scientia News who offer strategies to build confidence and reframe negative thinking. Acknowledging imposter syndrome is the first step, but learning to challenge it is what truly allows you to move forward. And the next time you begin to doubt yourself, take a step back and think about your achievements and how they themselves were born from the ashes of self-doubt. Written by Jaspreet Mann Related articles: My role as a clinical computer scientist / Mental health strategies / Mental health in South Asian communities REFERENCES “Imposter Syndrome: A Curse You Share with EinsteinThesislink « Thesislink.” Thesislink, 10 July 2018, https://thesislink.aut.ac.nz/?p=6630 . NHS Inform (2023) ‘Imposter syndrome’, NHS Inform. Available at: https://www.nhsinform.scot/healthy-living/mental-wellbeing/stress/imposter-syndrome . Mind (2022) ‘Understanding imposter syndrome’, Mind. Available at: https://www.mind.org.uk/information-support/types-of-mental-health-problems/imposter-syndrome/ . Healthline (2021) ‘What is imposter syndrome and how can you combat it?’, Healthline. Available at: https://www.healthline.com/health/mental-health/imposter-syndrome . Psychology Today (2020) ‘Overcoming imposter syndrome’, Psychology Today. Available at: https://www.psychologytoday.com/gb/blog/think-well/202002/overcoming-imposter-syndrome . beanstalk. Feel Like a Fraud? How to Overcome Imposter Syndrome - Employee and Family Resources . 1 Jan. 2023, https://efr.org/blog/feel-like-a-fraud . Ling, Ashley. “3 Ways to Get Past Imposter Syndrome.” Thir.St , 13 Aug. 2024, https://thirst.sg/3-ways-to-get-past-imposter-syndrome/ . Project Gallery

Many commercial activities are negative, particularly the production and marketing of ultra-processed foods (UPFs), which have contributed to a global obesity crisis. Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Dessert deception: how junk food advertising affects public health Last updated: 29/05/26, 18:22 Published: 04/06/26, 08:00 Many commercial activities are negative, particularly the production and marketing of ultra-processed foods (UPFs), which have contributed to a global obesity crisis. Introduction Chocolate. Crisps. Popcorn. If you're living in the UK, these are things you will no longer see on TV before 9 pm and in paid-for online advertising. This is because the UK has recently implemented a landmark ban on junk food advertisements, with the aim of making unhealthy food less desirable and therefore less consumed by the public. However, research from the World Health Organisation (WHO) suggests that marketing restrictions are only one small part of a strategy to combat the global rise in obesity. Unfortunately, eating habits are no longer just a matter of individual choice: they are increasingly being affected by commercial determinants of health. Researchers have defined them as "strategies and approaches used by the private sector to promote products and choices that are detrimental to health". While some commercial activities can be positive, many are negative, particularly the production and marketing of ultra-processed foods (UPFs), which have contributed to an obesity crisis globally. Frontier Economics calculated the cost of obesity to be approximately £74 billion a year for the UK in an analysis for the Tony Blair Institute, of which the cost to the NHS is more than £11 billion. The science of "engineered" cravings A review from Harvard, Michigan, and Duke University suggests that many UPFs share more characteristics with tobacco cigarettes than with natural foods like fruit or vegetables. The research identified some key strategies used by both the food and tobacco industries to drive addiction and compulsive consumption. They are "dose optimisation", "speed of delivery", "hedonic engineering" and "deceptive reformulation", seen in Table 1 . Table 1 - A comparison of key strategies used by both the food and tobacco industries to drive addiction and compulsive consumption. Source: https://onlinelibrary.wiley.com/doi/10.1111/1468-0009.70066 Strategy UPFs (ultra-processed foods) Cigarettes Dose optimisation UPFs are calibrated to hit a "hedonic sweet spot" of refined carbohydrates and added fats that maximise reward without causing aversion. Nicotine dose is standardised in cigarettes that maximise reward without causing aversion. Speed of delivery Processing techniques break down the food matrix, stripping away fibre and protein so that carbohydrates, sugar and added fats are instantly absorbed into the bloodstream. Additives are used to further increase the absorption speed and efficiency. This rapid delivery triggers a sharper dopamine surge in the brain's reward pathways, increasing the potential for addiction. Industrial processing breaks down the tobacco plant matrix, making it easy to rapidly absorb nicotine through inhalation, with additives added to increase nicotine's speed of delivery. Hedonic engineering Companies add artificial flavours, sweeteners, colourants and more to create "flavour bursts" that fade quickly, intentionally added to encourage repeated intake and amplify appeal. Cigarettes contain flavourings, menthol, and sweeteners for the same reason. Deceptive reformulation UPFs are marketed using "health-washing" claims and terms like "lighter", "low-fat", "sugar-free" and "vitamin-enhanced" to deflect regulation while maintaining addictive properties. Companies market "light" cigarettes and filters as being safer, even though they are still addictive. The UK's landmark 2026 junk food advertising ban On 5 January 2026, the UK implemented a nationwide ban on television and online advertisements for products high in fat, salt, and sugar (HFSS). This ban prohibits junk food ads on TV before the 9 pm watershed and imposes a total ban on paid-for online advertising. The legislation targets the most vulnerable demographic: children, whose developing dietary habits are easily manipulated by high-energy and colourful branding. The UK government expects this action to remove up to 7.2 billion calories from UK children's diets every year, reduce the number of children living with obesity by 20,000 and deliver approximately £2 billion in health benefits over time. The ban is supported by evidence from the National Child Measurement Programme's annual report for the academic year 2024/2025 , which shows that at the start of primary school, approximately 10% of children in England are already living with obesity. This figure rises to more than 22% by the time children leave primary school, as seen in Figure 1 . However, while public health experts have said that the ban is "long overdue", they warn that industry loopholes are undermining its effectiveness. In the UK, while specific products like pizzas or burgers are banned, the "brand-only" exemption allows companies to advertise their brand (e.g., the McDonald's "Golden Arches") as long as specific HFSS products aren't shown. This has led to a shift in marketing strategy: research from the Food Foundation shows that food companies increased their outdoor advertising spend, including billboards and public transport, by 28% between 2021 and 2024. Examples can be seen in Figure 2a and Figure 2b . McDonald's alone has spent £86 million on outdoor ads in 2024, up 71% since 2021, according to the Health Foundation . The WHO's perspective on why pricing matters While the UK focuses on advertising, the WHO warns that harmful products are becoming cheaper globally. Recent WHO reports reveal that weak tax systems are failing to keep pace with inflation and income growth, making sugary drinks and alcohol more affordable than they were years ago. Due to this, the WHO advocates for health taxes as one of the strongest tools for promoting well-being. Dr Tedros Adhanom Ghebreyesus, WHO Director-General, explains that "health taxes are one of the strongest tools we have for promoting health and preventing disease". In the UK, the 2018 Soft Drinks Industry Levy is cited as a major success; it generated £338 million in revenue in 2024 and has been associated with lower obesity rates in girls, particularly in deprived areas. However, the WHO notes that globally, sugary drink taxes often account for only 2% of the retail price, which is far too low to be effective compared to the 50-60% tax rates seen on tobacco. To address this, the WHO launched the "3 by 35" initiative , aiming to significantly increase the real prices of tobacco, alcohol, and sugary drinks by at least 50% by 2035 through tax increases. The economic win Contrary to industry arguments that these restrictions harm the economy, new research from the Sheffield Addictions Research Group suggests that reducing consumption of unhealthy products is actually a net economic gain for the UK. Because money spent on local services stays in the UK and money spent on global junk food brands often goes to the companies, reallocating just 10% of spending from confectionery to other domestic sectors could boost the UK economy by £389 million and create nearly 7,000 new jobs. Conclusion The UK's 2026 ban on junk food adverts is a significant step towards holding the food industry accountable. However, this must be seen as the first of many steps, rather than a final solution. While the ban restricts TV and online ads, industry giants are already exploiting loopholes to maintain their influence over people's food preferences, especially children's. To achieve its ambition of raising the healthiest generation of children ever, the UK must acknowledge that many UPFs are not just poor dietary choices but industrially engineered substances designed to influence human biology and drive compulsive consumption, much like tobacco. A truly effective strategy requires a whole systems approach that moves beyond individual responsibility to food industry accountability. This includes closing loopholes in outdoor advertising and sports sponsorship, and implementing health taxes aligned with the WHO's "3 by 35" initiative that rise with inflation to ensure harmful products do not become more affordable over time. Instead of harming finances, this shift is actually a significant economic win. This means transitioning from a model of "treating sickness" to one of active prevention is not just a public health imperative; it is also a strategic investment in the country's long-term economic and social prosperity. Written by Naoshin Haque Related articles: Rising food prices / Food at the molecular level / Childhood obesity Project Gallery

An analysis of risk and protective factors Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Postpartum depression in adolescent mothers Last updated: 24/06/25, 17:39 Published: 10/07/25, 08:00 An analysis of risk and protective factors Impact and prevalence According to the DSM-5, postpartum depression (PPD), also known as postnatal depression, is characterised by psychological and physical symptoms – including anhedonia, depressed mood and abnormal differences in sleep patterns – with a postpartum onset within one month after childbirth. Long-term effects of PPD, which are the same for adult and adolescent mothers, include weaker attachment between the mother and the child and developmental delays in children. Whilst treatment methods for postnatal depression have been more thoroughly investigated in adult mothers than in teenage mothers, prevalence rates of postpartum depression are found to be higher in adolescent mothers, with teenage mothers being twice as likely to be depressed as adult mothers. Postpartum depression in adolescent mothers is a prominent concern, as studies have found that up to 57% of teenage mothers report moderate to severe symptoms of PPD. Risk and protective factors A definite risk factor for postpartum depression in teenage mothers is a lack of social support. Research shows that adolescent mothers face more challenges but have fewer resources and less social support than adult mothers. This is prominent in Barnet et al.’s (1996) research, which found that adolescent mothers who received emotional support from either their mother or the baby’s father were less likely to exhibit depressive symptoms postpartum. Others support this research and suggest that social support has a direct effect on PPD in teenage mothers. Additionally, a lack of wider social support results in stigma, with a common assumption being that young mothers are incompetent parents and that children should not raise other children. Thus, another aspect of the lack of social support that might lead to PPD is stigma. However, an abundance of social support can also be detrimental, as it might make the young mothers feel incapable or inadequate, also leading to postnatal depression. Therefore, it is vital to determine the appropriate amount of support required for adolescent mothers. Another important risk factor affecting adolescent mothers that leads to postpartum depression is stress, which can be, but does not have to be, caused by a lack of social support. Research shows that higher stress levels are positively associated with depressive symptoms, and teenage mothers who reported higher stress levels displayed higher levels of PPD than adolescent mothers with lower stress levels. Therefore, in order to reduce the rate of postpartum depression in adolescent mothers, interventions should focus on decreasing the mothers’ stress levels. A crucial protective factor for PPD in adolescent mothers is self-esteem. Logsdon et al. (2005) found that lower self-esteem was predictive of postnatal depression in teenage mothers, and Caldwell & Antonucci (1997) found that self-esteem has a strong negative correlation with PPD symptoms in adolescent mothers. Therefore, higher self-esteem can shield young mothers from postpartum depression. Conclusions Overall, adolescent mothers are a particularly vulnerable population due to the additional challenges they face and the common lack of preparation for motherhood amongst teenage mothers. Social support, both a lack thereof or an excess amount, is commonly identified in the literature as a key risk factor for PPD in young mothers, as well as stigma and stress. High self-esteem and confidence in one’s own parenting skills are prominent and promising protective factors. The few interventions that are present demonstrate a promising start towards developing ways to tackle PPD in adolescent mothers. However, there has not been an extensive meta-analysis evaluating existing interventions, a clear limitation and a gap in the literature that should be addressed in future research. Written by Aleksandra Lib Related articles: Depression / Depression in children / Childhood stunting / Gynaecology REFERENCES American Psychiatric Association (APA). (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Barnet, B., Joffe, A., Duggan, A. K., Wilson, M. D., & Repke, J. T. (1996). Depressive symptoms, stress, and social support in pregnant and postpartum adolescents. Archives of pediatrics & adolescent medicine , 150 (1), 64-69. Caldwell, C. H., Antonucci, T. C., Jackson, J. S., Wolford, M. L., & Osofsky, J. D. (1997). Perceptions of parental support and depressive symptomatology among black and white adolescent mothers. Journal of Emotional and Behavioral Disorders , 5 (3), 173-183. Deal, L. W., & Holt, V. L. (1998). Young maternal age and depressive symptoms: Results from the 1988 National Maternal and Infant Health Survey. American Journal of Public Health, 88 , 266–270 Dinwiddie, K. J., Schillerstrom, T. L., & Schillerstrom, J. E. (2017). Postpartum depression in adolescent mothers. Journal of Psychosomatic Obstetrics & Gynecology , 39 (3), 168–175. Field T. (1992). Infants of depressed mothers. Development and Psychopathology, 4 , 49-66. Logsdon, M. C., Birkimer, J. C., Simpson, T., & Looney, S. (2005). Postpartum depression and social support in adolescents. Journal of Obstetric, Gynecologic & Neonatal Nursing , 34 (1), 46-54. Radke-Yarrow, M., Cummings, E. M., Kuczynski, L., & Chapman, M. (1985). Patterns of attachment in two- and three-year-olds in normal families and families with parental depression. Child Development, 56 , 886-893. Schmidt, R. M., Wiemann, C. M., Rickert, V. I., & Smith, E. O. B. (2006). Moderate to severe depressive symptoms among adolescent mothers followed four years postpartum. Journal of Adolescent Health , 38 , 712–718. Project Gallery

Explaining The Pain Gate Theory Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Gatekeepers of pain: how your body decides what hurts Last updated: 18/09/25, 09:40 Published: 18/09/25, 08:00 Explaining The Pain Gate Theory Pain is an unpleasant bodily sensation that’s usually linked to actual or potential tissue damage. It often acts as the body’s warning system, protecting us from further harm. Now picture this: you hit your leg, and it hurts—but then you instinctively start rubbing it, and the pain begins to ease. Why does that happen? That’s where the Pain Gate Theory (also known as The Gate Theory of Pain, or The Gate Control Theory of Pain) comes in. It’s one of the most fascinating ideas in pain science because it explains how pain isn’t just about injury— it’s also about how our nervous system processes it. Pain can vary greatly between individuals and even in the same person under different circumstances. This variation is due to the fact that pain is not just a physical experience, but also influenced by emotions, attention, and context. The Pain Gate Theory was first coined in 1965 by Ronald Melzack and Patrick Wall to explain this phenomenon. It states that a stimulus must travel through the substantia gelatinosa in the dorsal horn of the spinal cord, the transmission cells and the fibres in the dorsal column in order to have an effect. The substantia gelatinosa acts as a ‘gate’, mediating which signals are able to pass through the nervous system to the brain. As to whether the gate closes is influenced by an array of factors. How does it work? The below figure depicts the relationships in The Pain Gate Theory. The gate mechanism is influenced by the activity of the larger diameter fibres (A-beta) which usually inhibit transmission and the small diameter fibres (A-delta and C) which increase transmission. Take our analogy from earlier about rubbing your leg: when you do this, the large fibres carrying non painful stimuli like touch and pressure are activated. This causes the gate to be ‘closed’ which blocks the pain signals being transmitted by the small fibres. This concept is so interesting as it opens doors to viewing pain holistically; pain is influenced by touch, thoughts and emotions, which explains why you may not notice pain as much when your super excited about something or why placebos have been proven to work in some cases. In a clinical sphere, this theory has opened the door to many pain management techniques, for example Transcutaneous Electrical Nerve Stimulation (TENS), which selectively stimulates A-beta fibres leading to a consequential inhibition in A-delta and C fibres, preventing pain-related signals reaching the brain. It also has been utilised in physiotherapy, labour and chronic pain treatments. One main limitation of this model is its inability to explain certain types of pain like phantom limb since it relies on the assumption that pain requires an input from a limb to the spinal cord . This has led to the development of more advanced models like the neuromatrix model which acknowledges the fact that the brain can create pain on its own. In conclusion, the bottom line is that The Pain Gate Theory was groundbreaking in our understanding of how pain works. Understanding pain as a brain-and-body experience opens the door to innovative treatments that may one day make pain more manageable, or even preventable. Written by Blessing Amo-Konadu Related articles: Ibuprofen / Anthrax toxin to treat pain REFERENCES Cho, In-Chang, and Seung Ki Min. “Proposed New Pathophysiology of Chronic Prostatitis/Chronic Pelvic Pain Syndrome.” Urogenital Tract Infection , vol. 10, no. 2, 2015, p. 92, https://doi.org/10.14777/uti.2015.10.2.92 . Accessed 29 June 2020. Merrick, Mark. “Gate Control Theory - an Overview | ScienceDirect Topics.” Sciencedirect.com , 2012, www.sciencedirect.com/topics/medicine-and-dentistry/gate-control-theory . Tashani, O, and M Johnson. “Transcutaneous Electrical Nerve Stimulation (TENS). A Possible Aid for Pain Relief in Developing Countries?” Libyan Journal of Medicine , vol. 4, no. 2, 10 Dec. 2008, pp. 77–83, www.ncbi.nlm.nih.gov/pmc/articles/PMC3066716/pdf/LJM-4-062.pdf , https://doi.org/10.4176/090119 . The British Pain Society. “What Is Pain?” Britishpainsociety.org , July 2020, www.britishpainsociety.org/about/what-is-pain/ . Trachsel, Lindsay A., et al. “Pain Theory.” PubMed , StatPearls Publishing, 17 Apr. 2023, www.ncbi.nlm.nih.gov/books/NBK545194/ Project Gallery

Looking at caspase-8’s inability to trigger cell death Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link CEDS: a break in cell death Last updated: 08/10/26, 19:00 Published: 11/09/25, 08:00 Looking at caspase-8’s inability to trigger cell death This is article no. 11 in a series on rare diseases. Next article: Comparing types of treatments for NMO . Previous article: Ehlers-Danlos syndrome . Cell death, as we know it, is a crucial phenomenon by which our bodies remove unnecessary or damaged cells to maintain internal stability, a process known as homeostasis. Cell death can occur in many ways, but the mechanisms by which cells die follow two main paths. It may occur as naturally programmed, as in apoptosis, or as a result of toxic trauma or physical damage, like necrosis. While cell death due to trauma can often be more noticeable and dramatic, programmed cell death happens continually, not only because of cell damage but also because it is a normal part of development, and inducing it is a core function of immune system cells. In essence, cell death comes naturally, removing cells that are possibly damaged or infected to maintain the body as a whole. But what if cell death stops? As many fiction stories will tell you, immortality is never a good thing, and this is accurate for our cells, too. Although excessive cell death is also destructive, cell death in its natural controlled manner not only stops the spread of infection but also prevents the survival of cancer cells and auto-reactive immune cells, which can damage the body by forming cancerous tumours and triggering autoimmune diseases, respectively. This demonstrates that a careful balance of life and death must always be in place to maintain homeostatic conditions and allow our unimpeded survival. However, as cell death is a multi-step mechanism, it can go wrong in several ways. Furthermore, diseases causing faults in the cell death process can be challenging to diagnose. Not only can there be numerous reasons for patients to exhibit symptoms associated with the loss of cell death, but some of these reasons may also be rare disorders and, therefore, difficult for healthcare professionals to identify. One rare disease that researchers recently recognised is Caspase-8 Deficiency Syndrome (CEDS). This disease, stemming from a genetic mutation in the gene coding for caspase-8, results in extensive issues related to immunodeficiency, and they are all caused by caspase-8’s inability to trigger cell death. So what is Caspase-8? Caspase-8 is a pivotal regulator of the apoptotic pathway. Essentially, apoptosis can happen through two key pathways: the extrinsic pathway, when triggers originate outside the cell; and the intrinsic pathway, when the cell itself activates the cell death pathway. Whilst there are several key players in apoptosis, caspase-8 is a central mediator of the extrinsic apoptotic pathway. Caspase-8 can be activated through numerous ways, but it is often through so-called death receptors, which are typically members of the Tumour Necrosis Factor Receptor (TNFR) family of transmembrane proteins. Upon their activation, a chain reaction occurs, involving the recruitment of caspase-8 into a complex, known as the death-inducing signalling complex (DISC). This complex then cleaves further downstream caspases or the BH3 Bcl2-interacting protein. This cascade leads to DNA fragmentation, degradation of the cytoskeleton, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors, and finally, uptake by phagocytes, thus completing the death of the cell and its cleanup ( Figure 2. ). Caspase-8 therefore plays a crucial role in completing the death inducing pathway. While there are other methods of cell death, the loss of Caspase-8 undoubtedly leads to significant consequences. Caspase-8 deficiency syndrome (CEDS) Scientists first discovered CEDs in the early 2000s. By this time, there had already been extensive research into a similar disease known as Autoimmune Lymphoproliferative Syndrome (ALPS), which results from defective apoptosis leading to abnormal immune cell survival. However, at the time of ALPS discovery, there was no identified link to a loss of Caspase-8. Furthermore, there was a lack of available mouse models to study, as inducing homozygous caspase-8 deficiency caused embryonic lethality in mice, significantly limiting research. Therefore, a loss of caspase-8 was also considered to have the same effect in humans. This train of thought continued until 2002, when Chun et al. conducted major studies into apoptosis-related diseases. During one of their many trials, two siblings—a 12-year-old girl and an 11-year-old boy—were found to exhibit symptoms similar to those of ALPS (lymphadenopathy, splenomegaly, and defective CD95-induced apoptosis of peripheral blood lymphocytes). However, unlike ALPS, the siblings were also immunodeficient and suffered from recurrent sinopulmonary and herpes simplex virus (HSV) infections, as well as a poor response to immunisation. Following the discovery of these additional symptoms in the siblings, researchers examined their other family members but were surprised to find that neither the parents nor another sibling suffered in a similar fashion. The only symptom they had was a partial defect in apoptosis mediated by CD95. It was determined that the mother, father, sibling, and several other extended family members were potentially heterozygous carriers of the mutation found in the affected siblings. Subsequently, a DNA analysis was conducted, and a mutation was found in the CASP8 gene. This mutation was a homozygous deletion, which ultimately led to a loss of function of the caspase-8 protein. This loss of function in caspase-8 resulted in defective interleukin 2 production and diminished T-cell proliferation, explaining the immunodeficiency associated with CEDS and highlighting the important role caspase-8 plays in regulating cell death and immune responses. Since CEDS was first identified in the 2002 study, very few cases have been reported in medical literature. However, despite this, research continues, and it has allowed further insights into caspase-8’s pathophysiology and, in many studies, new genetic variants have been identified. One such variant is a homozygous missense mutation resulting in significant immune dysregulation in an affected individual, which results in immune responses and inflammatory conditions associated with the disease. Alongside research into the causes of this disease, focus has also shifted to how we might best diagnose and treat the disease and provide patients with the good quality of life they deserve. Diagnosis As with all rare diseases, one of the main issues stopping correct diagnosis of CEDS and delaying treatment is the fact healthcare providers are not familiar with disease symptoms, let alone the genetic basis of the disease. To make matters worse, the presentation of disease varies depending on the age of onset, which makes it even more difficult to recognise CEDS as the common underlying cause. For instance, early-onset often results in symptoms, such as severe infections and organomegaly, while adult-onset patients may present with neurological issues, multi-organ failure and chronic inflammatory conditions. Further adding to these diagnostic difficulties is the fact CEDS overlaps with other conditions, such as the previously mentioned ALPs. As a result, a patient could receive multiple different diagnoses before CEDS is identified as the cause of their suffering. For effective CEDS diagnosis, expertise in immunology, genetics and infectious diseases is required. However, this specialised knowledge is hard to come by, and as with all diseases, the familiarity the healthcare provider has with it contributes greatly to whether you will get diagnoses, and this familiarity does not exist for rare diseases. Furthermore, diagnostic methods in general are tricky for this disease, with multiple tests often being required including an analysis of patient history alongside genetic testing through methods like whole exome sequencing and immunological tests analysing the types and states of immune cells and abnormal levels of immunoglobulins. Each of these diagnostic methods takes time, in an often-strained healthcare system, which can lead to a sense of helplessness in disease sufferers who only suffer more the longer they do not know what is wrong. Treatments Unfortunately for patients, a difficult diagnosis is not the only challenge they face, as there is currently no cure for CEDS, and no specific treatments. However, there are more general treatments available that could potentially alleviate symptoms and help individuals achieve some level of normality in their lives. The best possible way to approach treatment of CEDS, as with most immunodeficiency related diseases, would be to treat both the immune dysfunction and prevent recurrent infections. This could involve a multifaceted treatment plan tailored to the individual, aiming to avoid complications from immune dysfunction and improve quality of life. Potential treatment plans could include the use of antibiotic and antiviral medications for recurrent infections, and also more complex treatments such as Immunoglobulin replacement therapy (IVIG). IVIG provides necessary antibodies to bolster patients’ immune system, when they are not able to themselves, which both helps avoid overuse of antibiotic and antiviral treatments and prevents infections in the first place before treatment is required. Alongside these treatment methods, due to it being a relatively unknown disease, CEDS patients will also require a great deal of supportive and hands on care. As part of this care patients could potentially be provided with a specialised diet plan with all the correct nutrition to help them combat any gastrointestinal issues (GI’s) associated with CEDS, as primary immunodeficiency patients have found this method to help with control of GIs. In addition to current therapies several innovative approaches to treatment of genetic diseases are in development which could be used in CEDS treatment. Recent advances in gene therapy research offer new hope for treating immune deficiencies resulting from genetic defects, which means these therapies could potentially benefit CEDS patients. One promising method for gene therapy utilises CRISPR-Cas9 to correct the genetic mutations, such as those in CASP8 leading to CEDS. Another approach uses viral vectors to deliver functional genes into patients’ cells, and this could potentially deliver a functional CASP8 gene. Additionally, another very promising therapy, previously used for ALPS patients, involves genetically modifying stem cells to correct a faulty gene (such as the faulty CASP8 gene) before re-infusing them into the patient to produce healthy immune cells. These treatments could revolutionise the management of rare genetic diseases like CEDS. The future for CEDS as a rare disease Rare diseases like CEDS are often chronic and, in many cases, life threatening. Due to the scarcity of information on these conditions, few if any treatments exist. Furthermore, due to their rarity, patients of rare diseases are not only small in number but also dispersed worldwide, leading to a feeling of isolation as they rarely meet someone who shares in their experiences. However, as scientific research progresses, treatments and therapies become more effective and accessible, and with 72% of rare diseases, including CEDS, having a genetic basis, gene therapies appear incredibly promising. Yet, there is still a long way to go to fully realize their potential, and even more that can be done to help and support those who continue to suffer alone with rare diseases. Written by Faye Boswell REFERENCES Telford WG. Multiparametric analysis of apoptosis by flow cytometry. Methods Mol Biol. 2018;1678:167–202. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC8063493/ Smith C. Monitoring apoptosis by flow cytometry. Biocompare. 2017 Jan 17. Available from: https://www.biocompare.com/Editorial-Articles/332620-Monitoring-Apoptosiby-Flow-Cytometry/ Tummers B, Green DR. Caspase-8; regulating life and death. Immunol Rev. 2017 May;277(1):76–89. doi: 10.1111/imr.12541. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC5417704/ Leeies M, Flynn E, Turgeon AF, Paunovic B, Loewen H, Rabbani R, Abou-Setta AM, Ferguson ND, Zarychanski R. High-flow oxygen via nasal cannulae in patients with acute hypoxemic respiratory failure: a systematic review and meta-analysis. Syst Rev. 2017 Oct 18;6(1):202. doi: 10.1186/s13643-017-0607-1. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4439260/ Goyal A, Moitra D, Goldstein DB, Savage H, Lisco A, Rosenzweig SD, et al. Caspase-8 deficiency presenting as a novel immune dysregulation syndrome: case report and literature review. Allergy Asthma Clin Immunol. 2023;19(1):57. doi:10.1186/s13223-023-00778-3. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10084589/ Chun HJ, Zheng L, Ahmad M, Wang J, Speirs CK, Siegel RM, et al. Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency. Nature. 2002 Sep 26;419(6905):395–9. doi:10.1038/nature01063. Available from: https://pubmed.ncbi.nlm.nih.gov/12353035/ Khan S, Saha S, Saha S, et al. Early and frequent exposure to antibiotics in early childhood and risk of overweight: a systematic review and dose-response meta-analysis. Obes Rev. 2021;22(3):e13113. doi:10.1111/obr.13113. Available from: https://www.gastrojournal.org/article/S0016-5085(18)35036-4/fulltext Casanova JL, Abel L. Caspase-8 deficiency syndrome. Front Immunol. 2019;10:104. doi:10.3389/fimmu.2019.00104. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7750663/ Castiello MC, Villa A. Stem cell editing repairs severe immunodeficiency. The Scientist. 2024 Mar 6. Available from: https://www.the-scientist.com/stem-cell-editing-repairs-severe-immunodeficiency-71733 Ha TC, Morgan M, Schambach A. Base editing: a novel cure for severe combined immunodeficiency. Signal Transduct Target Ther. 2023;8(1):354. doi:10.1038/s41392-023-01586-2. Available from: https://www.nature.com/articles/s41392-023-01586-2https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7750663/ Project Gallery

How music can manipulate our emotional processes Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The cognitive orchestra Last updated: 17/06/25, 12:21 Published: 26/06/25, 08:00 How music can manipulate our emotional processes Introduction Music has considerably always been a universal way of communicating. Every day, we are introduced to new genres and concepts despite the differences in language or musical techniques. As a result, psychology has increasingly researched music and its effects on human cognition. Music as a means of therapy The common way most people use music is to regulate their emotions. When we are feeling down, we are more than likely to choose a melancholic playlist over an upbeat one. It has been found that music aids in uplifting mood and reducing anxiety. Juslin and Sloboda (2010) demonstrated that people often choose to listen to music that links to how they are feeling in the moment or even how they desire to feel. With music being deemed a powerful emotional mechanism, music therapy has seen its benefits as a tool for regulating emotions. Thoma et al. (2013) support the idea of music being used for treating conditions like depression and PTSD, with their findings indicating that music listening impacts the psychobiological stress system. Listening to music prior to a stressful event predominantly affected the autonomic nervous system by recovering the nerves much faster, although the effects on the physiological stress and the endocrine (stress hormones) were not as noticeable. However, just as all forms of therapy are not generalisable to everyone, music therapy is not always an appropriate solution. The over-reliance on music to regulate feelings can lead to emotional avoidance and not addressing the initial cause of low mood. This leaves no room for solving the issues at hand. In the context of neurological rehabilitation, it was suggested that further controlled studies are needed to establish the efficacy of music in neurological recovery, and music-based interventions are emerging as promising rehabilitation strategies. Mental clarity or spiritual melodies? The benefits music can hold for our cognitive abilities are endless. Musical training in childhood, studied by Forgeard et al. (2008), is positively correlated with enhanced fine motor skills and non-verbal reasoning. Children were predicted to have much better cognitive flexibility and strengthened memory, outperforming the experimental control group. Another advantage music holds for cognitive abilities is making tasks easier to work with. Lesiuk (2005) conducted a study into the influence of music on mood and work performance. He introduced a ‘no music’ rule for workers in a software company, where they were prohibited from listening to music whilst working. The results demonstrated a predictable decrease in quality of work once music was abandoned, which workers were not habitually familiar with. Performance in quality of work remained poor in week 4, but managed to improve again when music was involved again during week 5. Although, it is important to note that music as a means of concentrating is not always beneficial. Lyrical songs can potentially act as a distractor when completing tasks that require verbal or visual memory, hindering our cognitive ability. Zulkurnaini et al. (2012) studied Lesiuk (2005) hypothesis, exposing participants to classical music and a verse from the Quran. By observing EEG signals, they found that listening to the Quran resulted in a more relaxed state compared to classical music. They also found that listening to the Quran increased the alpha band in the brain, which is associated with relaxation. Conclusion It is clear music is more than just a background track while completing daily errands. The influence it has on emotional well-being, memory and mood is vital to acknowledge. With evidence of positive correlations between cognitive productivity and listening to music, and neurological research of in-depth brain studies, the effects of music are much more prevalent to us. Future research should aim to look into the long-term effects on cognitive functioning, more specifically within clinical settings like neurorehabilitation. Written by Tania Khan Related article: Chemistry of emotions REFERENCES Schäfer, T., Sedlmeier, P., Städtler, C., & Huron, D. (2013). The psychological functions of music listening. Frontiers in Psychology, 4 , 511. Juslin, P. N., & Sloboda, J. A. (2010). Music and emotion. In P. N. Juslin & J. A. Sloboda (Eds.), Handbook of Music and Emotion: Theory, Research, Applications (pp. 3-20). Oxford University Press. Thoma, M. V., La Marca, R., Brönnimann, R., Finkel, L., Ehlert, U., & Nater, U. M. (2013). The effect of music on the human stress response. PLOS ONE, 8 (8), e70156. Krause, A. E., North, A. C., & Heritage, B. (2023). The role of music listening in reducing stress and anxiety: A meta-analysis. PLOS ONE, 18 (1), e0281337 Lesiuk, T. (2005). The effect of music listening on work performance. Psychology of Music, 33 (2), 173-191. Lesiuk, T. (2012). The effect of music listening on work performance. IEEE Transactions on Professional Communication, 55 (4), 282-290. Lesiuk, T. (2005). The effect of music listening on work performance. PLOS ONE, 8 (8), e70156. Miller, A. H., Haroon, E., Raison, C. L., & Felger, J. C. (2017). Cytokine targets in the brain: Impact on neurotransmitters and neurocircuits. The Lancet Neurology, 16 (11), 1013-1025. Project Gallery

Arginine, the key to metabolic reprogramming in liver cancer Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Linking arginine and tumour growth: a breakthrough in cancer research Last updated: 20/02/25, 15:29 Published: 27/02/25, 08:00 Arginine, the key to metabolic reprogramming in liver cancer Unpicking the secrets of tumour growth: arginine, the key to metabolic reprogramming in liver cancer. We will look at how unleashing the power of arginine and elevating levels of this amino acid drive metabolic reprogramming and fuel tumour growth. Introduction In recent years, the field of cancer research has made significant progress in unravelling the complexities of this devastating disease. Scientists at the University of Basel have made a groundbreaking discovery regarding the role of the amino acid arginine in promoting tumour growth. Their findings shed light on the mechanisms underlying metabolic reprogramming in cancer cells and present new avenues for improving liver cancer treatment. Elevated levels of arginine: a surprising revelation An intriguing aspect of the study conducted by the researchers is the observation that tumour cells accumulate high levels of arginine despite producing less or none of this amino acid. Through careful analysis of liver tumour samples from both mice and patients, the team discovered that the tumour cells achieve this accumulation by increasing the uptake of arginine and suppressing its consumption. The role of arginine in tumorigenicity Upon further investigation, the scientists at the University of Basel found that high concentrations of arginine bind to a specific factor, triggering metabolic reprogramming in the tumour cells. This reprogramming, in turn, promotes tumour growth by regulating the expression of metabolic genes. The tumour cells revert to an undifferentiated embryonic cell state, enabling them to divide indefinitely. Immune system escape: a beneficial effect for tumour cells Another fascinating discovery made by the researchers is the role of arginine in aiding tumour cells in evading the immune system. Immune cells rely on arginine to function properly. By depleting arginine in the tumour environment, the tumour cells can escape immune surveillance. This finding opens up new possibilities for targeted therapies. Targeting the arginine-binding factor: a novel approach Instead of depleting arginine levels overall, which can have unwanted side effects, the scientists propose targeting the specific arginine-binding factor responsible for promoting metabolic reprogramming. By inducing the degradation of this factor, the researchers were able to prevent metabolic reprogramming in liver tumours. This approach offers a promising alternative to liver cancer treatment. Metabolic changes as biomarkers for early cancer detection Furthermore, the study suggests that metabolic changes, such as increased arginine levels, may serve as biomarkers for the early detection of cancer. Early detection is crucial for successful cancer treatment and patient survival. This finding provides hope for the development of non-invasive diagnostic methods that can detect elevated arginine levels. By measuring arginine levels in patients, these diagnostic methods can potentially identify liver cancer at an early stage. By identifying the elevated levels of arginine in liver tumour cells, these diagnostic methods could potentially use metabolic changes, such as increased arginine levels, as biomarkers for detecting cancer. Therefore, this would be crucial for successful cancer treatment and patient survival, as early detection allows for prompt intervention and improved outcomes. Conclusion The discovery of the role of arginine in driving metabolic reprogramming and promoting tumour growth opens up new avenues for liver cancer treatment. Additionally, the elevated levels of arginine observed in liver cancer patients suggest the potential for using arginine as a biomarker for non-invasive cancer detection. Further research is needed to explore the full potential of arginine as a diagnostic marker and to develop targeted therapies that exploit the metabolic vulnerabilities of cancer cells. With continued advancements in our understanding of cancer metabolism and the role of arginine in tumour growth, further research is needed to explore the full potential of arginine as a diagnostic marker and to develop targeted therapies that exploit the metabolic vulnerabilities of cancer cells. By studying the specific arginine-binding factor and its role in promoting metabolic reprogramming, scientists may be able to develop new treatments that selectively target tumour cells while minimising harm to immune cells that rely on arginine. Additionally, investigating the metabolic changes associated with increased arginine levels may lead to new biomarker designs for early cancer detection, which is crucial for successful treatment and patient survival. Written by Sara Maria Majernikova Related articles: Immune signals and metastasis / Cancer research treatment / Prostatate cancer treatment REFERENCE MOSSMANN, D., MÜLLER, C., PARK, S., RYBACK, B., COLOMBI, M., RITTER, N., WEISSENBERGE, D., DAZERT, E., COTO-LLERENA, M., NUCIFORO, S., BLUKACZ, L., ERCAN, C., JIMENEZ, V., PISCUOGLIO, S., BOSCH, F., TERRACCIANO, L. M., SAUER, U., HEIM, M. H. & HALL, M. N. Arginine reprograms metabolism in liver cancer via RBM39. Cell . DOI: https://doi.org/10.1016/j.cell.2023.09.011 Project Gallery