Discussing eutrophication and industrial activities Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How human activity impacts the phosphorus cycle Last updated: 27/12/25, 17:55 Published: 15/01/26, 08:00 Discussing eutrophication and industrial activities Phosphorus is one of the most important chemical elements in biology because it is a component of nucleic acids, ATP, and the phospholipid bilayers that make up our cell membranes. Like carbon and nitrogen, there is a limited amount of phosphorus on Earth, which is continually cycled between inorganic, organic, terrestrial, and aquatic sources. However, human activity disrupts the phosphorus cycle, resulting in some places having too much phosphorus and others having too little. This article will describe what the phosphorus cycle is and how we are affecting it. What is the phosphorus cycle? The phosphorus cycle involves phosphate ions (PO 4 3- ) moving between rocks, living organisms, and water bodies. Phosphate enters ecosystems when wind and rain break off tiny pieces of phosphate rock, primarily apatite, in a process called weathering. Weathered phosphate rock enters soil, where micro-organisms transform it into a form that plants can absorb through their roots (see my previous article on this process, called phosphate solubilisation). Plants convert inorganic phosphate into organic phosphorus compounds, such as DNA, ATP, and phosphoproteins, which are then transferred along the food chain. At each step of the food chain, phosphorus is returned to the soil by excretion from living organisms or decomposition of dead organisms. I call this the ‘organic mini-cycle’ from soil, to plants, to animals, and back to soil. Occasionally, phosphorus leaves the organic mini-cycle and enters water bodies by leaching or soil erosion. Phosphorus settles on the seabed and turns back into phosphate rock over hundreds of millions of years, completing the cycle. An overview is shown in Figure 1 . Humans disrupt the phosphorus cycle by eutrophication Deforestation, farming, and sewage overload water bodies with nutrients like phosphorus in a process called eutrophication. Agriculture is a big source of eutrophication, specifically fertilisers, organophosphorus pesticides, and animal feed. When it rains, they are carried from farm soil to water bodies by surface runoff and soil erosion. Human-caused deforestation exaggerates eutrophication because without tree roots, soil erosion increases, so more agricultural phosphorus enters water bodies. The other big eutrophication source is domestic sewage, which is dumped directly into water bodies. Fertilisers, pesticides, animal feed, and sewage provide algae with excess nutrients, so they overgrow into an algal bloom ( Figure 2 ). Algal blooms block sunlight from reaching submerged aquatic plants, so they cannot photosynthesise, and may produce toxins that kill aquatic life. Once the algal bloom dies, it is decomposed by bacteria, which use up oxygen in the water. With oxygen used up and no photosynthesis to replace it, fish and other aquatic animals die. Therefore, human phosphorus inputs like fertilisers and domestic waste can destroy aquatic ecosystems. Industrial activity depletes non-renewable phosphate rock While human activities overload water bodies with phosphorus, they deplete land of phosphate rock. Phosphate rock is mined and chemically reacted with sulfuric acid to produce fertiliser. Since phosphate rock is non-renewable, mining it permanently removes a crucial phosphorus input from the local ecosystem. 85% of phosphate rock is found in only 5 countries (China, Morocco, South Africa, Algeria, and Syria), so these countries are being depleted of phosphorus, only to overload another ecosystem with fertiliser thousands of miles away ( Figure 3 ). Scientists have suggested using agricultural waste and domestic wastewater as an alternative phosphorus source for fertiliser production. This would rebalance the phosphorus cycle on both ends: reducing the demand for non-renewable phosphate rock, and preventing eutrophication. Phosphorus can be recovered from waste and reused in fertiliser production in a variety of ways – acid leaching, isolating iron phosphate using a magnet, metal precipitation, and polyphosphate-accumulating micro-organisms, which use and store phosphate in their cells. However, the pollution and diseases present in sewage and farm waste make them difficult to recycle. Conclusion Phosphorus is an essential element for plant growth, so humans have manufactured fertilisers to provide their crops with extra phosphorus. However, fertiliser production depletes some ecosystems of phosphate rock, while fertiliser application causes eutrophication in other ecosystems. Along with domestic sewage and deforestation, agriculture has disrupted the natural cycle, which transports phosphate between plants, animals, micro-organisms, the soil, water bodies, and rocks. Therefore, making fertiliser by recycling the phosphorus in our waste products could keep the human population fed without compromising natural ecosystems. Written by Simran Patel Related article: Meet the microbes that feed phosphorus to plants REFERENCES Schipanski ME, Bennett EM. Chapter 9 - The Phosphorus Cycle. In: Weathers KC, Strayer DL, Likens GE (eds) Fundamentals of Ecosystem Science (Second Edition) . Academic Press, pp. 189–213. R. Jupp A, Beijer S, C. Narain G, et al. Phosphorus Recovery and Recycling – Closing the Loop. Chemical Society Reviews 2021; 50: 87–101. Khan MN, Mohammad F. Eutrophication: Challenges and Solutions. In: Ansari AA, Gill SS (eds) Eutrophication: Causes, Consequences and Control: Volume 2 . Dordrecht: Springer Netherlands, pp. 1–15. Akinnawo SO. Eutrophication: Causes, consequences, physical, chemical and biological techniques for mitigation strategies. Environmental Challenges 2023; 12: 100733. Liu L, Zheng X, Wei X, et al. Excessive Application of Chemical Fertilizer and Organophosphorus Pesticides Induced Total Phosphorus Loss from Planting Causing Surface Water Eutrophication. Sci Rep 2021; 11: 23015. Project Gallery

Unveiling the paradigm shift in cognitive impairment through machine learning Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Brain metastasis hacks brain activity and jams neuronal communication Last updated: 29/05/25, 11:46 Published: 29/05/25, 08:00 Unveiling the paradigm shift in cognitive impairment through machine learning Understanding the impact of brain metastasis on neuronal communication Introduction Researchers from the Spanish National Research Council (CSIC) and the Spanish National Cancer Research Centre (CNIO) have made a ground-breaking discovery related to brain metastasis and its impact on brain activity and neuronal communication. This finding could potentially explain why half of all patients with brain metastasis experience cognitive impairment. Understanding the influence on neural circuits The research , published in Cancer Cell, aimed to comprehend how brain metastasis affects the functionality of neuronal circuits beyond the physical mass of the tumour. The researchers conducted multidimensional modelling of brain functional analyses in the context of brain metastasis and tested various preclinical models from different primary sources and oncogenic profiles. The study was able to separate the effect on local field potential oscillatory activity from cortical and hippocampal areas. This helped researchers learn more about the different ways that brain metastasis can affect people. The authors highlighted the importance of this comprehensive approach in unravelling the complex dynamics of brain metastasis. Detecting metastases through electrical activity Through the measurement of electrical activity in the brains of mice with and without metastases, the researchers discovered distinct electrophysiological differences between the two groups. The researchers used artificial intelligence to confirm that metastases were indeed to blame for these differences. Using an automatic algorithm trained with numerous electrophysiological recordings, the researchers developed a model that could accurately identify the presence of metastases. Furthermore, the algorithm demonstrated the ability to distinguish metastases originating from different primary tumours, such as skin, lung, and breast cancer. These findings provide clear evidence of the specific impact that metastasis has on the brain's electrical activity. Paradigm shift in understanding brain metastases The study represents a significant paradigm shift in the understanding of brain metastases. Traditionally, neurological dysfunction in patients with brain metastasis was attributed solely to the physical mass effect of the tumour. However, this research indicates that changes in brain activity resulting from tumour-induced biochemical and molecular alterations also contribute to these symptoms. The implications of this paradigm shift are far-reaching and have potential implications for the prevention, early diagnosis, and treatment of brain metastasis. By recognising that neurological symptoms are not solely due to the physical presence of the tumour, medical professionals can explore novel diagnostic and therapeutic strategies. Potential therapeutic targets Looking ahead, the researchers are eager to explore potential therapeutic targets that can protect the brain from cancer-induced disruptions in neuronal circuits. They aim to identify molecules involved in metastasis-induced changes in neuronal communication, intending to evaluate them as possible therapeutic targets. The researchers want to create strategies that might stop or lessen the neurological dysfunction that patients frequently experience by understanding the biochemical and molecular changes brought on by brain metastasis. This could lead to advancements in the prevention, early diagnosis, and treatment of brain metastasis, ultimately improving patient outcomes. Conclusion The groundbreaking studies carried out by the Spanish National Research Council and the Spanish National Cancer Research Centre have shed light on how brain metastasis affects brain activity and neuronal communication. By dissociating the effects of tumour mass from changes in brain activity, the study has revealed the complex dynamics of brain metastasis and its contribution to cognitive impairment in patients. The discovery of distinct electrophysiological differences and the development of an algorithm to detect metastases offer promising opportunities for early diagnosis and personalised treatment. This paradigm shift in understanding brain metastases opens the door for novel diagnostic and therapeutic strategies, as well as the exploration of potential therapeutic targets to protect the brain from cancer-induced disruptions. With further research, it is hopeful that advancements in the prevention, early diagnosis, and treatment of brain metastasis will improve patient outcomes and lead to a better understanding of neurological dysfunction in these patients. Written by Sara Maria Majernikova Related articles: Cancer on the move / Cancer magnets / Latent space transformations / Uploading brain to a computer REFERENCE Sanchez-Aguilera A, Masmudi-Martín M, Navas-Olive A, Baena P, Hernández-Oliver C, Priego N, Cordón-Barris L, Alvaro-Espinosa L, García S, Martínez S et al : Machine learning identifies experimental brain metastasis subtypes based on their influence on neural circuits . Cancer Cell 2023, 41 (9):1637-1649.e1611. Project Gallery

Causes, symptoms, diagnosis and management Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Hypertension: a silent threat to global health Last updated: 08/10/26, 18:58 Published: 13/03/25, 08:00 Causes, symptoms, diagnosis and management Introduction Did you know that hypertension, also known as high blood pressure, is a leading cause of premature death, affecting 1.28 billion adults aged 30-79 worldwide? According to the World Health Organisation (WHO), two-thirds of these individuals live in low and middle-income countries. Despite its widespread prevalence, many people remain undiagnosed as most cases are asymptomatic, and individuals are unaware they have the condition. Hypertension can lead to serious clinical manifestations such as heart disease. It can also cause eye retinopathy, causing vision problems and kidney damage, including proteinuria. It also contributes to vascular contributions like atherosclerosis, leading to stenosis and aneurysms. It also significantly raises the risk of stroke and heart failure (Figure 1 ). Addressing hypertension through early diagnosis, improved access to treatment and lifestyle changes is essential to reducing its global burden. This article aims to explore the causes, diagnosis and treatments. What drives hypertension? Hypertension is characterised by persistently elevated BP in the systemic arteries. Blood pressure is typically presented as a ratio: systolic BP, which measures the pressure on arterial walls during heart contraction, and diastolic BP, which reflects the pressure when the heart is at rest. Hypertension is diagnosed when the systolic blood pressure is 130 mmHg or higher and/or diastolic blood pressure exceeds 80 mmHg based on multiple readings taken over time ( Figure 2 ). In contrast, secondary hypertension occurs only in 5% of cases and is caused by an underlying condition, such as kidney disease, hormonal imbalances, or vascular problems. This form of hypertension is often reversible if the underlying cause is treated. Common causes of secondary hypertension include chronic kidney disease, polycystic kidney disease, hormone excess (such as aldosterone and cortisol), vascular issues like renovascular stenosis and certain medications. Drugs that can cause secondary hypertension include chronic use of non-steroidal inflammatory drugs (NSAIDs), antidepressants and oral contraceptives. Hypertension, regardless of its cause, can be exacerbated by certain health behaviours, including excessive dietary salt, a sedentary lifestyle, heavy alcohol consumption, and diets low in essential nutrients, such as potassium. These factors contribute to the development and worsening of high blood pressure. However, blood pressure can be improved by reversing these behaviours, as well as following a diet rich in fruits and vegetables, which helps to mitigate the negative impact on blood pressure. Spotting hypertension: how it is diagnosed Hypertension is usually detected when blood pressure (BP) is measured during regular checkups. Since it often doesn’t show symptoms, all adults must check their BP regularly. The most common way to diagnose hypertension is by measuring BP several times in a doctor’s office. To get an accurate reading, BP must be measured carefully. Since BP can vary throughout the day, multiple measurements are needed. Doctors have recently started using home BP monitoring (HBPM) and ambulatory BP monitoring (ABPM) to check BP outside of the office. ABPM records BP every 20-30 minutes over 24 hours, while HBPM lets patients measure BP at home. These methods help identify conditions like 'white coat hypertension' (high BP in the doctor’s office but normal at home) or 'masked hypertension' (normal BP at the doctor’s office but high at home). When diagnosing hypertension, doctors also look for other health issues related to high BP, such as heart disease or kidney problems. If high BP is sudden or difficult to control, doctors may suspect secondary hypertension, which is caused by another condition, like kidney disease or hormonal imbalances. A thorough medical history is essential. This includes asking about past BP readings, medications, and lifestyle factors such as smoking and diet. Doctors also check for other risk factors like diabetes or high cholesterol, increasing heart disease risk. A physical exam helps confirm the diagnosis of hypertension and checks for any damage to organs like the heart and kidneys. BP should be measured on both arms and if there's a significant difference in readings, further tests may be needed. If necessary, doctors may also check for conditions like atrial fibrillation or perform ultrasounds to look for heart or kidney problems. Blood tests can also help identify risk factors, confirm or rule out secondary hypertension, and assess overall heart health. Managing hypertension, from lifestyle changes to medications Studies show that weight loss can reduce systolic blood pressure by 5 to 20 mmHg, making it an effective strategy for managing hypertension. However, the exact "ideal" body weight or Body Mass Index (BMI) for controlling blood pressure is not clearly defined, but small weight reductions can make a difference. Reducing salt intake, staying active, and managing sleep apnoea also help. While smoking does not directly raise blood pressure, quitting reduces long-term heart risks. Overall, lifestyle changes alone can cut cardiovascular events by up to 15%. Most national and international guidelines recommend the use of angiotensin-converting enzyme inhibitors (ACE inhibitors), angiotensin II receptor blockers (ARBs), calcium channel blockers (CCBs), and thiazide or thiazide-like diuretics as first-line pharmacological treatments for hypertension. Conclusion Hypertension is a prevalent and often silent condition with serious health consequences, including heart disease, stroke, and kidney failure. Its widespread impact on global health, particularly in low- and middle-income countries, underscores the importance of early diagnosis and proactive management. While lifestyle modifications are crucial in managing blood pressure, medications remain essential for many individuals. By raising awareness, promoting regular blood pressure checks, and ensuring access to both preventative and therapeutic measures, we can reduce the burden of hypertension and improve long-term health outcomes globally. Written by Michelle Amoah Related articles: Related mechanisms of hypertension / Cardiac regeneration REFERENCES Iqbal, A. M., and Jamal, S. F. (2023). Essential hypertension. In StatPearls [Internet]. StatPearls Publishing. Retrieved from [ https://www.ncbi.nlm.nih.gov/books/NBK539859/ ] Schmieder, R. E. (2010). End Organ Damage In Hypertension. Deutsches Ärzteblatt International. https://doi.org/10.3238/arztebl.2010.0866 Touyz, R. M., Camargo, L. L., Rios, F. J., Alves-Lopes, R., Neves, K. B., Eluwole, O., Maseko, M. J., Lucas-Herald, A., Blaikie, Z., Montezano, A. C., and Feldman, R. D. (2022). Arterial Hypertension. In Comprehensive Pharmacology (pp. 469–487). Elsevier. World Health Organization. (2023). Hypertension. Retrieved [24th January 2025], from https://www.who.int/news-room/fact-sheets/detail/hypertension Project Gallery

Seizures are not mainly uncontrolled jerking and losing consciousness Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Epilepsy 101: what are the different types of epilepsy seizures? Last updated: 29/04/25, 17:09 Published: 27/02/25, 08:00 Seizures are not mainly uncontrolled jerking and losing consciousness After previously covering a very generic overview into epilepsy – what it is, its different types, methods of diagnosis and treatment, it would be a good idea to really delve deeper into the different types of seizures. Are they just convulsions, shaking and losing consciousness? Or is there more to it? Read more to find out! But before we begin, it is important to cover some key terms and prefixes, to help us with understanding what the different types of seizures are: Myo-: muscle Clonic: repeated jerking Tonic: muscle stiffness Atonic: muscles become limp Motor: movement From our previous article , we know that the two main types of epilepsy are generalised and focal epilepsy. Each type of epilepsy has different types of seizures associated with it. Generalised epilepsy – it consists of 2 main types of seizures (motor and non-motor seizures): 1) Generalised Motor Seizures: Involves changes in muscle activity, where they either move abnormally, or don’t move at all. This includes: Myoclonic seizures: sudden body jerks (especially the hands or the legs) as if someone had been jolted with electricity. Tonic - Clonic (Grand mal) seizures: This seizure has 2 main phases – a tonic and clonic stage:- Initial tonic (stiffness) phase is followed by a clonic (repeated, uncontrolled jerking of the limbs) phase. During the 'tonic' phase, the person may become unconscious and fall to the floor. In the 'clonic' phase, the person might struggle to breathe or uncontrollably bite their tongue. This is probably the ‘typical’ seizure everyone thinks of when they hear about epilepsy! Atonic seizures: The muscles become limp, and the person might even collapse. 2) Generalised non-motor seizures: They are usually also referred to as 'absence seizures', and they don’t include any changes in muscle activity. Instead, the person might stare into space, and might have a pause in activity, or a repetition in movements, such as lip-smacking for around 15 seconds or less. The individual may not remember what happened during the seizure; however their normal state of alertness is regained immediately after. People might easily confuse this type of seizure with daydreaming! Focal epilepsy- This is split into 4 main types based on whether the person is aware of their seizure, and if there are any changes in muscle activity involved: 1) Focal awareness seizures: Patient is fully aware of what is happening during a seizure, even if they are unable to move or respond. Some people might experience an "aura" as a warning before this seizure. This could feel like a strange sensation, fear, euphoria, a sense of déjà vu, feeling that something bad is about to happen, visual changes or even tingling or stiffness in their body. 2) Focal impaired awareness seizures: The person isn’t aware of their seizure, nor can they remember having it, and can’t respond to anyone during the seizure. The seizure can include movements such as moving their hands and legs or making random noises. 3) Focal Motor Seizures: involves random muscle activity, such as twitching, stiffness, limpness, or other movements such as rubbing hands, lip-smacking and walking around. 4) Focal Non-motor Seizures: no muscle movements or stiffness (as this is a non-motor seizure), but there is a change in a patient’s feelings and thoughts, causing strange feelings, a racing heart, and waves of heat or cold. Now that we’ve covered the key seizures, what triggers epilepsy seizures, causing those lights in the city (which in this case, is our brain) to start flickering or shut completely? There are many different causes, and they vary from one person to another. They could include: Stress Lack of sleep Drinking alcohol Consuming illegal drugs Not taking your anti-seizure medication (ASMs) Some types of medication Menstrual Cycle and hormonal changes Flashing lights (for individuals with photosensitive epilepsy) Photosensitive epilepsy is epilepsy that is triggered by flashing of lights, causing seizures such as myoclonic seizures. It is interesting to see how many people hold the misconception that seizures are mainly uncontrolled jerking and losing consciousness, when in fact there’s a huge variety of seizure! It is important that we know what different seizures look like, so we could help these individuals appropriately. Don’t be afraid to read further about epilepsy and seizures, and how to help people out there! Written by Hanin Salem Related articles: Epilepsy 101 (overview) / Traumatic brain injuries REFERENCES Dhanyamraju, S. (2019). What is a Seizure? - Lone Star Neurology . [online] Lone Star Neurology. Available at: https://lonestarneurology.net/seizures/seizures/ . [Accessed 19 Dec. 2024]. Ditki medical & biological sciences. (n.d.). Neurological System Glossary: Tonic-Clonic Seizure . [online] Available at: https://ditki.com/course/neurological-system/glossary/eeg-findings/tonic-clonic-seizure . [Accessed 19 Dec. 2024]. Epilepsy action (2022). Focal seizures | Epilepsy Action . [online] www.epilepsy.org.uk . Available at: https://www.epilepsy.org.uk/info/seizures/focal-seizures [Accessed 18 Dec. 2024]. John Hopkins Medicine (n.d.). Generalized Seizures . [online] Available at: https://www.hopkinsmedicine.org/health/conditions-and-diseases/epilepsy/generalized-seizures#:~:text=Generalized%20seizures%20include%20absence%2C%20atonic [Accessed 17 Dec.2024]. NHS (2020). Symptoms - Epilepsy . [online] NHS. Available at: https://www.nhs.uk/conditions/epilepsy/symptoms/ [Accessed 17 Dec. 2024]. Project Gallery

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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, 15:16 Published: 03/07/25, 08:00 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

Observations suggest that aspects of their design were purposeful for other reasons Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The astronomical symbolism of the Giza Pyramids Last updated: 09/10/25, 11:03 Published: 06/03/25, 08:00 Observations suggest that aspects of their design were purposeful for other reasons This is Article 2 in a series about astro-archaeology. Next article: The celestial blueprint of time: Stonehenge, UK . Previous article: Cities designed to track the heavens: Chaco Canyon, New Mexico The Giza Pyramids of the ancient Egyptian civilisation may be most well known as one of the Seven Wonders of the Ancient World, but they also harbour astronomical secrets. The three Great Pyramids (Khafre, Khufu, and Menkaure) are incredible feats of engineering, with heights measuring 146.6 meters, 143.5 meters, and 64.5 meters, respectively. No documentation has been found explaining the planning or construction processes behind the creation of these magnificent structures, yet observations suggest that aspects of their design were purposeful for reasons other than simply erecting the pyramid. Example 1: The square bases of the pyramids are very carefully oriented to the cardinal points with the Khufu Pyramid aligning within 4 arc minutes of the north-south line. For context, if you were to hold your index finger up, it would cover a portion of the sky that measures about 10 degrees across. 1 arc minute is a unit of measurement equal to 1/60 of 1 degree, which means that the orientation of the Khufu Pyramid only deviates from the north-south line by less than 4/60-degree error. Today, we would calculate this using a GPS or other technical equipment, but what did the ancient Egyptians use? Well, astronomy! While the exact method of calculation is not known, researchers believe that the ancient engineers aligned the pyramids to the constellation Orion and the star Sirius as they are circumpolar stars, never rising nor setting, and are therefore visible every night as a useful guide. This may also have religious implications relating to immortality, perhaps adding to the desire to align the Pharoah’s tombs with such a symbolic constellation. Example 2: The south-eastern corners of the three Giza Pyramids all point toward the nearby great solar temple of Heliopolis, which was a major religious centre of the sun god Atum-Ra. According to the Pyramid Texts, Heliopolis was the location that the god-creator Atum emerged from chaos and begun creation. These texts suggest that the ancient Egyptians believed that the Pharaohs join Atum-Ra in the afterlife, and they together cross the sky in Atum-Ra’s sun boat as part of the rebirth process. Upon investigation, the three pyramids seem to be aligned with various solar events as well as the city of the sun god: the setting sun is aligned with the northern side of the Khafre pyramid and the southern side of the Khufu pyramid during the equinoxes the causeways point to the setting sun behind the pyramid twice per year, which are distanced the same number of days from the winter/summer solstices each of the two causeways point towards sunset in two separate locations that are halfway between the equinoxes and solstices, respectively (not according to the calendar year, but according to the astronomical year) on the summer solstice, the sun sets directly between the two great pyramids when viewing from the Sphinx area of the pyramidal complex Example 3: the position of three Great Pyramids with respect to each other mimics the position of the stars in the constellation Orion’s belt with respect to each other. Astronomical calculations show that the orientation and position of the Khufu, Khafre, and Menkaure pyramids align together in exactly the same way that the Alnitak, Alnilam, and Mintaka stars align in Orion’s belt. Of course, there is a small percentage of error, but it is because of naked eye observations instead of mathematical miscalculations. While there are still many secrets hidden in and around the Great Pyramids of ancient Egypt, they can continue to provide insight into how ancient peoples interconnected architecture, astronomy/mathematics, and religious beliefs within their societies. Written by Amber Elinsky REFERENCES Magli, G. (2009). Archaeoastronomy at Giza: the ancient Egyptians’ mathematical astronomy in action. In: Emmer, M., Quarteroni, A. (eds) Mathknow. MS&A, vol 3. Springer, Milano. https://doi.org/10.1007/978-88-470-1122-9_10 . Orofino, V. and P. Bernardini. Archaeoastronomical Study of the Main Pyramids of Giza, Egypt: Possible Correlations with the Stars?. Archaeological Discovery: 1 (2016), vol 3. https://www.scirp.org/journal/paperinformation?paperid=61389 . Verner, Miroslav, 'Heliopolis: The City of the Sun', in Anna Bryson-Gustová (ed.), Temple of the World: Sanctuaries, Cults, and Mysteries of Ancient Egypt (Cairo, 2013; online edn, Cairo Scholarship Online, 18 Sept. 2014), https://doi.org/10.5743/cairo/9789774165634.003.0002 . https://pyramidtextsonline.com/translation.html 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, 08:00 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

Looking at how income and housing are linked to health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Socioeconomic Health Inequalities Last updated: 05/03/26, 14:50 Published: 05/02/26, 08:00 Looking at how income and housing are linked to health This is Article no. 2 in a series on health equalities. Previous article: What are health inequalities? Next article: Ethnic inequalities . Welcome to the second article in a series of articles about health inequalities. This article will look more in detail at what socioeconomic health inequalities are. Introduction Socioeconomic factors refer to the circumstances in which people are born, grow, live, work, and age. These conditions are often considered the wider determinants of health, and are a fundamental cause of health inequalities. These inequalities are not accidental; they are the result of underlying structural disparities, occurring as a result of unequal distribution of resources and opportunities in society. Addressing these disparities requires coordinated, cross-government action across a wide range of policy areas, including prevention and focused work on the wider determinants of health. How income is linked to health Poverty and financial insecurity have a significant negative impact on health, as living on a low income is a source of stress. It also affects an individual's ability to afford health-improving goods, from nutritious food to gym memberships. Across the income spectrum, lower incomes are associated with worse self-reported health. Data from the Department for Work and Pensions’ Family Resources Survey 2023/24 shows that 43% of people on the lowest income rate their health as fair, bad or very bad, compared with 31% in the middle (the fifth income decile) and 15% on the highest incomes. The Health Foundation has visualised this in Figure 1 . The impact on health is even greater when low pay persists for generations: children from households in the bottom fifth of income distribution are over 4 times more likely to experience severe mental health issues compared to those in the highest fifth. Furthermore, Black, Asian and Minority Ethnic (BAME) individuals are disproportionately affected and are more likely to live in poverty, have low incomes, and lower levels of wealth compared to White individuals. How housing links to health The places where people live and age can significantly influence their health. Affluent areas have more access to green and other public spaces, clean air, and affordable and active travel. In contrast, deprived areas often have less access to green space, higher concentrations of fast-food outlets, and limited availability of affordable and healthy food. Individuals living in deprived areas will most likely have poor-quality and overcrowded housing conditions, associated with an increased risk of cardiovascular and respiratory diseases, depression and anxiety. They may also experience fuel poverty, so they cannot afford to heat their home. BAME households are more likely than White households to live in overcrowded homes and to experience fuel poverty. Health outcomes and projections The consequences of socioeconomic inequalities can be seen in differences in health outcomes. People in more deprived areas experience major illness earlier in life and die younger: in England, individuals in the 10% most deprived areas are expected to develop major illness 10 years earlier compared to those in the 10% most affluent areas. They are also over three times more likely to die prematurely before the age of 70. This inequality is projected to continue through to at least 2040, with no expected improvement. These findings are supported by research which looked at the impact of socioeconomic factors on the COVID-19 pandemic. Results showed that unequal access to healthcare amplified COVID-19 cases. It meant that a significant portion of cases, which could have been prevented through timely diagnosis, treatment, and resource distribution, contributed to an overall case rate that was 6-fold higher than it otherwise might have been. Additionally, a small group of long-term conditions contributes to most diagnosed health inequalities: chronic pain, chronic obstructive pulmonary disease (COPD), type 2 diabetes, cardiovascular diseases (CVD), and anxiety and depression. The prevalence of these conditions is 1.5 times higher in the 10% most deprived areas compared to the least deprived areas. The Health Foundation has visualised this in Figure 2 . Conclusion Socioeconomic health inequalities are fundamentally caused by the structural inequalities discussed throughout this article. Actions to address these disparities must be specifically targeted in the most deprived areas, which often see a disproportionate impact on BAME individuals. The next article in this series will look more in detail at ethnic health inequalities, so watch out for that! Written by Naoshin Haque Related articles: Gentrification in the context of health / Global Health Injustices (series) Project Gallery

Research confirms anxiety disorders do have a genetic side Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Does anxiety run in families? Here's what genetics tells us Last updated: 10/07/25, 19:26 Published: 19/06/25, 08:00 Research confirms anxiety disorders do have a genetic side Have you ever noticed anxiety can pop up in several members of the same family? Maybe your sister worries constantly, or your brother gets nervous around people. It might feel like anxiety is passed down through generations. But is that really how it works, or is it just a coincidence? Here's what science has to say. Your DNA can affect anxiety Research confirms anxiety disorders do have a genetic side. That means you're more likely to have anxiety if someone in your family, like your mum, dad, sibling, or even a grandparent, has it too. But this doesn't mean anxiety is certain. Instead, genes increase your chances, accounting for about 30% to 40% of your risk. Scientists work this out by comparing identical and fraternal twins and by following anxiety diagnoses across generations; those studies repeatedly find that roughly one-third to two-fifths of a person’s risk is genetic. So, if genetics only make up part of the picture, what's the rest? That's where your environment steps in. Your life experiences matter a lot. Things like your relationships, stressful situations, and even your physical health can tip the scales one way or another. Genes set the stage, but they don't control the outcome. Think of your genes as nudging you towards anxiety rather than pushing you into it completely. The rest depends on what happens to you. How genes shape your brain Scientists have pinpointed several genes linked to anxiety. One of these genes affects serotonin, a brain chemical that helps regulate your mood and manage stress. When serotonin works well, you feel calm and can handle stressful events better. But if your genes make serotonin less effective, stress hits you harder. This can make anxiety more likely during tough times, even when others around you seem okay. There's another important point: your brain structure. Genes influence parts of your brain, especially the amygdala. Think of the amygdala as your internal alarm system. It warns you when something feels dangerous. In people with certain genes, the amygdala is extra sensitive. That means their "alarm" goes off more easily, causing anxiety even when there's no real danger present. However, not everyone with these genetic variations experiences anxiety. Your brain adapts throughout life, changing how genes affect you. This ongoing flexibility is called neuroplasticity: experience can strengthen or weaken neural circuits and can even add or remove chemical tags, such as DNA methylation, that switch genes on or off, reshaping how your stress system responds. Anxiety isn't just genetic; here's why It's tempting to blame your genes entirely if anxiety runs in your family. But life is more complicated. Even if you inherit genes that make anxiety more likely, the disorder usually develops when certain environmental conditions come into play. Stressful life events like losing a loved one, ongoing conflict at home, bullying, or trauma can trigger anxiety symptoms. Someone might have anxiety-related genes but never experience anxiety if their life stays relatively stress-free. On the other hand, someone without these genes can still develop anxiety if they experience severe stress or trauma. Lifestyle choices also make a big difference. Regular exercise, healthy eating, good sleep, and support from friends and family can protect against anxiety. Studies show these lifestyle habits are powerful, even if your genes are pushing in the opposite direction. Can you change your genetic destiny? Understanding that anxiety has a genetic basis can help. It means anxiety isn't just a character flaw or personal weakness. It's something partly built into your biology, something real and valid. Realising this can reduce shame and make people more willing to seek help. And here's another benefit: knowing your family history allows you to spot anxiety sooner. If you understand that anxiety might run in your family, you can pay attention to early signs, like trouble sleeping, excessive worry, or panic in social settings. Catching anxiety early means getting support earlier, making treatments like therapy or lifestyle changes more effective. Anxiety might run in your family, but you get to decide how far it goes. Written by Rand Alanazi Related articles: Depression / South Asian mental health / Physical and mental health / Does insomnia run in families? REFERENCES National Institute of Mental Health. Anxiety disorders [Internet]. Bethesda (MD): National Institute of Mental Health; 2024 [cited 2025 May 29]. Available from: https://www.nimh.nih.gov/health/topics/anxiety-disorders Mayo Clinic. Anxiety disorders [Internet]. Rochester (MN): Mayo Foundation for Medical Education and Research; 2018 [cited 2025 May 29]. Available from: https://www.mayoclinic.org/diseases-conditions/anxiety/symptoms-causes/syc-20350961 Leyfer O, Woodruff-Borden J, Mervis CB. Anxiety disorders in children with Williams syndrome, their mothers, and their siblings: implications for the aetiology of anxiety disorders. J Neurodev Disord . 2009 Feb 13;1(1):4-14. Martin EI, Ressler KJ, Binder EB, Nemeroff CB. The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. Psychiatr Clin North Am [Internet]. 2009 Sep;32(3):549-75. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684250/ McEwen BS, Eiland L, Hunter RG, Miller MM. Stress and anxiety: structural plasticity and epigenetic regulation as a consequence of stress. Neuropharmacology . 2012 Jan;62(1):3-12. Xie S, Zhang X, Cheng W, Yang Z. Adolescent anxiety disorders and the developing brain: comparing neuroimaging findings in adolescents and adults. Gen Psychiatry [Internet]. 2021 Aug 4;34(4):e100542. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8340272/ Zhang K, Ibrahim GM, Venetucci Gouveia F. Molecular pathways, neural circuits and emerging therapies for self-injurious behaviour. Int J Mol Sci [Internet]. 2025 Feb 24;26(5):1938. Available from: https://www.mdpi.com/1422-0067/26/5/1938 Chaves T, Fazekas CL, Horváth K, Correia P, Szabó A, Török B, et al. Stress adaptation and the brainstem with focus on corticotropin-releasing hormone. Int J Mol Sci [Internet]. 2021 Jan 1;22(16):9090. Available from: https://www.mdpi.com/1422-0067/22/16/9090 Project Gallery