Natural substances and their treatment potential Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Using Natural Substances to Tackle Infectious Diseases 05/04/26, 15:43 Last updated: Published: 06/06/23, 18:06 Natural substances and their treatment potential Introduction There is increased concern of antimicrobial resistance, especially when referring to bacteria with superbugs such as Methicillin-resistant Staphylococcus aureus (MRSA) and Carbapenem-resistant Enterobacteriaceae (CRE) as they impact lives globally, mainly through fatalities. Given this predicament, It seems that humanity is losing as a result of this pressing issue. However, it is possible for healthcare professionals to utilise more natural products, which are chemicals made by plants, animals and even microorganisms. This includes resources such as wood and cotton aside from food like milk and cacao. In the context of medicinal treatments, an important justification for using more natural products is because although synthetic or partially synthetic drugs are effective for treating countless diseases, an article found that 8% of hospital admissions in the United States and approximately 100,000 fatalities per year were due to people experiencing unfortunate side effects from these drugs. This article explores three specific natural products, where each have similar and unique health properties that can be harnessed to tackle infectious diseases and its subsequent consequences when left sufficiently unaddressed (i.e. antimicrobial resistance). Honey One of the most famous natural products that has been referenced in various areas of research and has been a food and remedial source for thousands of years is honey. It has properties ranging from antibacterial to antioxidant, suggesting that when honey is applied clinically, it has the potential to stop pathogenic bacteria. For example, honey can protect the gastrointestinal system against Helicobacter pylori , which causes stomach ulcers. In disc diffusion assays, the inhibitive properties of honey were shown when honey samples were evaluated holistically as opposed to its individual ingredients. This implies that the macromolecules in honey (carbohydrates, proteins and lipids) work in unison with other biomolecules, illustrating that honey is a distinctive remedy for preventing bacterial growth. For tackling infectious diseases, particularly against wound infections among others, honey’s medicinal properties provide a lot of applications and because it is a natural product, honey would not present any drastic side effects to a patient upon its administration. Garlic Another natural product that can be effective against microorganisms is garlic because similar to honey, it has antimicrobial and antioxidative compounds. A study judged different garlic phenotypes originating from Greece and discovered that they were beneficial against Proteus mirabilis and Escherichia coli aside from inhibiting Candida albicans and C. kruzei . As for fresh garlic juice (FGJ), it increases the zone of inhibition in various pathogens at 10% and more along with it displaying minimum inhibitory concentrations (MICs) in the 4-16% range. Therefore, garlic in solid or liquid form does show potential as a natural antimicrobial agent, especially against pathogenic bacteria and fungi. With this in mind, it too has multiple applications like honey and should be further studied to best isolate the chemical compounds that could be involved in fighting infectious diseases. Turmeric Curcuma longa (also known as turmeric) is one other natural product with unique properties like garlic and honey, making it a suitable candidate against various microbes. One specific pigment that is part of the ginger family and found in turmeric is curcumin, which can tackle diverse microbes through numerous mechanisms illustrated below in Figure 2 . With this said, curcumin has drawbacks: it is highly hydrophobic, has low bioavailability and quickly breaks down. Although when paired with nanotechnology for delivery into the human body, its clinical applications can be advantageous and an additional observation about curcumin is that it can work collaboratively with other plant derived chemicals to stop antibiotic resistant bacteria. One specific bacterial strain that turmeric can attack is Clostridium difficile, a superbug that causes diarrhoea. A study had 27 strains to measure the MICs of turmeric constituents, particularly curcuminoids and curcumin. The results showed reduced C. difficile growth in the concentration range 4-32 μg/mL. Moreover, they had no negative impacts on the gut microbiome and curcumin had more efficacy in stopping C. difficile toxin production compared to fidaxomicin. Thus, turmeric is efficacious as a natural antimicrobial chemical and with further experimentation (same as honey and garlic), it can be harnessed to prevent infectious diseases besides their impact on human lives. Conclusion Considering the above examples of natural products in this article and others not mentioned, it is clear that they can be powerful in the battle against infectious diseases and the problems associated with them, mainly antimicrobial resistance. They are readily available to purchase in markets and shops at low cost, making them convenient. Moreover, populations in Eastern countries like China and India traditionally have used, and are still using these materials for curing pain and illness. In turn, manufacturing medicines from natural products on a larger scale has the prospect of preventing infectious diseases and even alleviating those that patients currently have. Written by Sam Jarada Related article: Mechanisms of pathogen evasion Project Gallery

MIT scientists found reward sensitivity varies by socioeconomic status Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Motivating the Mind 08/02/25, 13:24 Last updated: Published: 22/04/24, 11:41 MIT scientists found reward sensitivity varies by socioeconomic status Behaviour is believed by many, including the famous psychologist B.F. Skinner, to be reinforced by rewards and the degree to which an individual is motivated by rewards is called reward sensitivity. Another common view is that behaviour is influenced by the environment, nowadays including socioeconomic status (SES). People with low SES encounter fewer rewards in their environment, which could affect their behaviour toward pursuing rewards due to their scarcity- Farah 2017. Thus, a study by Decker (2024) investigates the effect of low SES on reward sensitivity in adolescents through a gambling task, using fMRI technology to measure response times, choices and activity in the striatum – the reward centre of the brain. The researchers hypothesised that response times to immediate rewards, average reward rates and striatal activity would differ for participants from high compared to low SES backgrounds. See Figure 1 . The study involved 114 adolescents whose SES was measured using parental education and income. The participants partook in a gambling task involving guessing if numbers were higher or lower than 5, the outcomes of which were pre-determined to create blocks with reward abundance and reward scarcity. Low and high SES background teenagers gave faster responses and switched guesses when the rewards were given more often. Also, immediate rewards made the participants repeat prior choices and slowed response times. In line with the hypothesis, fewer adolescents with lower SES slowed down after rare rewards. Moreover, it was found that lower SES is linked with fewer differences between reward and loss activation in the striatum, indicating experience-based plasticity in the brain. See Figure 2 . Therefore, the research by Decker (2024) has numerous implications for the real world. As adolescents with lower SES displayed reduced behavioural and neural responses to rewards and, according to behaviourism, rewards are essential to learning, attention and motivation, it can be assumed that SES plays a role in the inequality in many cognitive abilities. This critically impacts the understanding of socioeconomic differences in academic achievement, decision-making and emotional well-being, especially if we consider that differences in SES contribute to prejudice based on ingroups and outgroups. Interventions to enhance motivation and engagement with rewarding activities could help buffer against the detrimental impacts of low SES environments on cognitive and mental health outcomes. Overall, this research highlights the need to address systemic inequities that limit exposure to enriching experiences and opportunities during formative developmental periods. Written by Aleksandra Lib Related article: A perspective on well-being REFERENCES Decker, A. L., Meisler, S. L., Hubbard, N. A., Bauer, C. C., Leonard, J., Grotzinger, H., Giebler M. A., Torres Y C., Imhof A., Romeo R. & Gabrieli, J. D. (2024). Striatal and Behavioral Responses to Reward Vary by Socioeconomic Status in Adolescents. The Journal of Neuroscience: the Official Journal of the Society for Neuroscience, 44(11). Farah, M. J. (2017). The neuroscience of socioeconomic status: Correlates, causes, and consequences. Neuron, 96(1), 56-71. Project Gallery

How your gut is your second brain (an opinion piece) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Microbes in charge Last updated: 16/06/25, 17:09 Published: 26/06/25, 08:00 How your gut is your second brain (an opinion piece) Imagine this: you have just won ten million dollars in the lottery, or you have just eaten the most delicious, warm, chocolate brownie. In these situations, our brains produce chemicals called neurotransmitters, which give us these great feelings of pleasure and happiness. Now, imagine this: you're about to sit an exam. In this situation, our brains, instead, produce different chemicals, making us feel stressed and anxious. Our emotions control the highs and lows of life. I have always heard that the brain inside all of us controls everything that we feel, think and do. However, I've always found it strange that every feeling, thought, and behaviour is controlled by a three-pound, soggy lump of cells inside our heads, until I learned about gut microbiota. We each have a second brain, which controls as much of our physical and mental functions as the brain in our heads, and plays a role in preventing diseases. This second brain is our gut microbiota. However, we have completely underestimated their role as the second brain. I learned this first through the intriguing story of the rat. If the rat becomes colonised with the microbe Toxoplasma gondii, a fascinating thing happens: they lose their fear of cats. The cat's smell was chosen as a measure. The infected rat preferred the areas that had the smell of cats. So, the microbes take control of the brain and change the way you think. In another study, a research group at University College Cork in Ireland fed Lactobacillus rhamnosus , a good bacteria—or 'probiotic' you can usually find in yoghurt—to one of two groups of mice. The probiotic mice were much more likely to succeed in the face of adversity tests than those not treated with the probiotic. They repeated a similar study in humans, with the probiotic-fed humans displaying improved resilience to negative emotions compared to those without the probiotic. As I mentioned earlier, neurotransmitters are these chemicals that can change how we think, behave, and feel. As it turns out, neurotransmitters are also produced in our gut, 50% of the dopamine and 90% of serotonin (nature's antidepressant): two neurotransmitters that drastically affect your mood, happiness and pleasure. According to some studies, dopamine also plays a role in memory and learning, so gut microbiota controls how you think and behave and is also involved in cognitive functions like memory and learning. Let’s now turn to mental health! One study by Venket Rao studied 39 individuals with chronic fatigue syndrome (a syndrome characterised by severe anxiety, depression, and long-term exhaustion), split the individuals into two groups. The first group received a bacterial strain for two months while the other group received only a placebo. The group that received the bacterial strain showed a significant decrease in anxiety with respect to the other group. Noticeably, there is a vital link between the gut microbiota and the immune system. 70-80% of immune cells are present in the gut. Additionally, studies have shown that Germ-free mice have fewer immune system structures in their intestines than wild-type mice. These immune structures in the gut are referred to as the gut-associated lymphoid tissues (GALT) and Peyer's patches. Another study explored the gut microbiota of 42 patients affected by Rheumatoid Arthritis and 10 healthy controls. They observed that rheumatoid arthritis patients have a higher population of Lactobacillaceae family and the Lactobacillus genus, and fewer Faecalibacterium , a butyrate producer. Butyrate is the fuel source for our intestinal cells to produce mucin, which then repairs the intestinal lining and mucosal membrane and reduces inflammation. Our gut and brain are physically and biochemically connected in several ways. First, our intestines are physically linked to our brain through the vagus nerve, which sends signals in both directions. Interestingly, even if this is cut off (severed), our intestines can continue to function fully without a connection to the brain, suggesting they have a mind of their own. Secondly, our brains are made up of a hundred billion neurons, which continuously send messages to tell our bodies how to work and behave. Well, interestingly, our guts have a hundred million neurons. Our gut microbiota, the unsung hero behind our feelings, thoughts, immune system and behaviour - proving that sometimes, it's not just all in our heads, but in our "guts" too! Written by Prabha Rana Related articles: The gut microbiome / The dopamine connection REFERENCES Webster J. P. (2007). The effect of Toxoplasma gondii on animal behavior: playing cat and mouse. Schizophrenia bulletin , 33 (3), 752–756. https://doi.org/10.1093/schbul/sbl073 Bravo, J. A., Forsythe, P., Chew, M. V., Escaravage, E., Savignac, H. M., Dinan, T. G., Bienenstock, J., & Cryan, J. F. (2011). Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve. Proceedings of the National Academy of Sciences of the United States of America , 108 (38), 16050–16055. https://doi.org/10.1073/pnas.1102999108 Strandwitz P. (2018). Neurotransmitter modulation by the gut microbiota. Brain research , 1693 (Pt B), 128–133. https://doi.org/10.1016/j.brainres.2018.03.015 Rao, A. V., Bested, A. C., Beaulne, T. M., Katzman, M. A., Iorio, C., Berardi, J. M., & Logan, A. C. (2009). A randomized, double-blind, placebo-controlled pilot study of a probiotic in emotional symptoms of chronic fatigue syndrome. Gut pathogens , 1 (1), 6. https://doi.org/10.1186/1757-4749-1-6 Wiertsema, S. P., van Bergenhenegouwen, J., Garssen, J., & Knippels, L. M. J. (2021). The Interplay between the Gut Microbiome and the Immune System in the Context of Infectious Diseases throughout Life and the Role of Nutrition in Optimizing Treatment Strategies. Nutrients , 13 (3), 886. https://doi.org/10.3390/nu13030886 Round, J. L., & Mazmanian, S. K. (2009). The gut microbiota shapes intestinal immune responses during health and disease. Nature reviews. Immunology , 9 (5), 313–323. https://doi.org/10.1038/nri2515 Picchianti Diamanti, A., Panebianco, C., Salerno, G., Di Rosa, R., Salemi, S., Sorgi, M. L., Meneguzzi, G., Mariani, M. B., Rai, A., Iacono, D., Sesti, G., Pazienza, V., & Laganà, B. (2020). Impact of Mediterranean Diet on Disease Activity and Gut Microbiota Composition of Rheumatoid Arthritis Patients. Microorganisms , 8 (12), 1989. https://doi.org/10.3390/microorganisms8121989 Han, Y., Wang, B., Gao, H., He, C., Hua, R., Liang, C., … Xu, J. (2022). Vagus Nerve and Underlying Impact on the Gut Microbiota-Brain Axis in Behavior and Neurodegenerative Diseases. Journal of Inflammation Research , 15 , 6213–6230. https://doi.org/10.2147/JIR.S384949 Project Gallery

How they're used in treatments Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A new model: miniature organs in biomedicine 23/10/25, 11:21 Last updated: Published: 16/10/23, 22:39 How they're used in treatments Introduction Within biomedicine, the study of diseases and understanding their mechanisms are crucial to the treatments we can develop for them. Before a treatment option can be rolled out to the general public, it must be tested for safety and efficacy. Usually, this testing takes place in the form of cell cultures or animal models. However, these methods cannot always accurately replicate the human body's complexity and physiological responses and are sometimes quite expensive and difficult to maintain. In the past few years, a new model has come to light known as organoids, allowing for a new realm of understanding into drug development, disease, and human biology. What Are Organoids? Organoids are self-organised, small, three-dimensional organ models which allow scientists and researchers to study different biological organs and tissues in a lab setting, including their physiological functions, development, and structure. These miniature organs are remarkable in their resemblance to actual organs and are obtained from stem cells, and they can undergo division to become any cell type. From their theoretical abilities, organoids may be able to serve utmost value in biomedicine and how we think about testing new treatments. Disease Modelling, Drug Development and Personalised Medicine One of the ways in which organoids can be used is to model diseases and test for potential drug targets and treatment programmes. In this way, researchers can replicate congenital and acquired conditions, such as cystic fibrosis and cancer, to study key target phenotypes and understand disease progression, which can help identify potential drug targets. From here, the efficacy of these therapeutics can be assessed quite quickly under different circumstances. As an example of this being used currently, scientists involved in cancer research have produced organoids from tumour cells stemming from cancer patients. These patient-derived organoids have been made for various cancers, including endometrium. They will allow for the ability to test chemotherapy drugs and determine which are most effective for individual patients whilst factoring in comorbidities and other unique factors to that person. Through this personalised approach, it is hoped that therapeutics will allow for a customised treatment programme which lowers the risk of side effects and improves the quality of care. Understanding Development and Function Another use of organoids is going into more depth and exploring our understanding of how an organ may develop and function. Using organoids can help us observe how different cells may work together and interact to organise themselves, allowing researchers to strengthen their knowledge of organogenesis by mimicking the natural growth conditions of the human environment. By combining tissue engineering with an appreciation of an organ's functional and developmental processes, organoid use can be extended to regenerative medicine to help fill research gaps in the molecular and cellular mechanisms of tissue regeneration. Techniques such as ELISA and immunofluorescent staining can help garner these critical details. By achieving this, organoids may produce entire organs for transplantation, addressing the organ donor shortage and lowering the risk of donor rejection. Recent Breakthroughs Cardiovascular diseases are one of the leading causes of death around the world. The human heart is limited to regenerating damaged tissue; thus, research must explore using organoids and other cell-based therapies to encourage natural repair processes. By investigating this avenue, cardiomyocytes derived from human pluripotent stem cells are a promising source. These cell types have the potential to restore contractile functions in animal models as well as the ability to regenerate myocardial tissue. Researchers have developed a cardiac organoid with silicon nanowires that have significantly improved the medicinal efficacy of stem cell-derived cardiac organoids. Using these nano-wired organoids, electrical activity was shown to improve, which in turn supported improved contractility in ischemia-injured mice. Challenges and Future Directions While the promising nature of organoids must be acknowledged, they are not without limitations. Research is currently ongoing to improve the reproducibility and scalability of organoids and their cultures to make organoids more accessible and their use more widespread. Below are some summarised advantages and disadvantages of organoids. Conclusion In conclusion, the advent of organoids has created a revolutionary era within the scope of biomedicine. These miniature organs have remarkable potential in various research, development, and tissue engineering facets. Organoids provide scientists with precise modelling of diseases across a range of different organs, assuring their versatility. From understanding organ development to combating cardiovascular diseases and introducing personalised treatment for cancer patients, it is unclear why they are being more rapidly explored. While they hold their promise, there are still challenges surrounding their reproducibility, restricting them from being used in organ transplantation. However, with ongoing progress, organoids undoubtedly have the aptitude to tailor treatments and address complexities of tissue regeneration, heralding a groundbreaking era in healthcare. Written by Irha Khalid Related article: iPSCs and organoids / Animal testing ethics Project Gallery

Causes, symptoms, diagnosis and management Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Hypertension: a silent threat to global health Last updated: 13/03/25, 11:38 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 article: 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

Deconstructing allergies: mechanisms, treatments, and prevention Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Allergies 08/07/25, 17:24 Last updated: Published: 13/05/24, 15:27 Deconstructing allergies: mechanisms, treatments, and prevention Modern populations have witnessed a dramatic surge in the number of people grappling with allergies, a condition that can lead to a myriad of health issues such as eczema, asthma, hives, and, in severe cases, anaphylaxis. For those who are allergic, these substances can trigger life-threatening reactions due to their abnormal immune response. Common allergens include antibiotics like penicillin, as well as animals, insects, dust, and various foods. The need for strict dietary restrictions and the constant fear of accidental encounters with allergens often plague patients and their families. Negligent business practices and mislabelled food have even led to multiple reported deaths, underscoring the gravity of allergies and their alarming rise in prevalence. The primary reason for the global increase in allergies is believed to be the lack of exposure to microorganisms during early childhood. The human microbiome, a collection of microorganisms that live in and on our bodies, is a key player in our immune system. The rise in sanitation practices is thought to reduce the diversity of the microbiome, potentially affecting immune function. This lack of exposure to infections may cause the immune system to overreact to normally harmless substances like allergens. Furthermore, there is speculation about the impact of vitamin D deficiency, which is becoming more common due to increased indoor time. Vitamin D is known to support a healthy immune response, and its deficiency could worsen allergic reactions. Immune response Allergic responses occur when specific proteins within an allergen are encountered, triggering an immune response that is typically used to fight infections. The allergen's proteins bind to complementary antigens on macrophage cells, causing these cells to engulf the foreign substance. Peptide fragments from the allergen are then presented on the cell surface via major histocompatibility complexes (MHCs), activating receptors on T helper cells. These activated T cells stimulate B cells to produce immunoglobulin E (IgE) antibodies against the allergen. This sensitizes the immune system to the allergen, making the individual hypersensitive. Upon re-exposure to the allergen, IgE antibodies bind to allergen peptides, activating receptors on mast cells and triggering the release of histamines into the bloodstream. Histamines cause vasodilation and increase vascular permeability, leading to inflammation and erythema. In milder cases, patients may experience itching, hives, and runny nose; however, in severe allergic reactions, intense swelling can cause airway constriction, potentially leading to respiratory compromise or even cessation. At this critical point, conventional antihistamine therapy may not be enough, necessitating the immediate use of an EpiPen to alleviate symptoms and prevent further deterioration. EpiPens administer a dose of epinephrine, also known as adrenaline, directly into the bloodstream when an individual experiences anaphylactic shock. Anaphylactic shock is typically characterised by breathing difficulties. The primary function of the EpiPen is to relax the muscles in the airway, facilitating easier breathing. Additionally, they counteract the decrease in blood pressure associated with anaphylaxis by narrowing the blood vessels, which helps prevent symptoms such as weakness or fainting. EpiPens are the primary treatment for severe allergic reactions leading to anaphylaxis and have been proven effective. However, the reliance on EpiPens underscores the necessity for additional preventative measures for individuals with allergies before a reaction occurs. Preventative treatment Young individuals may have a genetic predisposition to developing allergies, a condition referred to as atopy. Many atopic individuals develop multiple hypersensitivities during childhood, but some may outgrow these allergies by adulthood. However, for high-risk atopic children, preventive measures may offer a promising solution to reduce the risk of developing severe allergies. Clinical trials conducted on atopic infants explored the concept of immunotherapy treatments, involving continuous exposure to small doses of peanut allergens to prevent the onset of a full-blown allergy. Initially, skin prick tests for peanut allergens were performed, and only children exhibiting negative or mild reactions were selected for the trial. Those with severe reactions were excluded due to the high risk of anaphylactic shock with continued exposure. The remaining participants were randomly assigned to either consume peanuts or follow a peanut-free diet. Monitoring these infants as they aged revealed that continuous exposure to peanuts reduced the prevalence of peanut allergies by the age of 5. Specifically, only 3% of atopic children exposed to peanuts developed an allergy compared to 17% of those in the peanut-free group. The rise in severe allergies poses a growing concern for global health. Once an atopic individual develops an allergy, mitigating their hypersensitivity can be challenging. Current approaches often involve waiting for children to outgrow their allergies, overlooking the ongoing challenges faced by adults who remain highly sensitive to allergens. Implementing preventive measures, such as early exposure through immunotherapy, could enhance the quality of life for future generations and prevent sudden deaths in at-risk individuals. In conclusion, a dramatic surge in the prevalence of allergies in modern populations requires more attention from researchers and health care providers. Living with allergies can bring many complexities into someone’s life even before they potentially have a serious reaction. Currently treatments are focused on post-reaction emergency care, however preventative strategies are still a pressing need. With cases of allergies predicted to rise further, research into this global health issue will become increasingly important. There are already promising results from early trials of immunotherapy treatments, and with further research and implementation these treatments could improve the quality of life of future generations. Written by Charlotte Jones Related article: Mechanisms of pathogen evasion Project Gallery

Richard Dawkins's work and the Modern Evolutionary Synthesis Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Is the immune system ‘selfish’? – a Dawkins perspective Last updated: 26/04/26, 15:38 Published: 25/09/25, 08:00 Richard Dawkins's work and the Modern Evolutionary Synthesis Evolution and Dawkins’ perspective Charles Darwin introduced the unprecedented theory of evolution by natural selection in his famous work ‘On the Origin of Species’, published in 1859. Gregor Mendel, who explained the concept of Mendelian genetics (the inheritance of genes), was a contemporary of Darwin, but his research was recognised much later on, beyond his time. In the 20 th century, the Modern Evolutionary Synthesis was formed and gave a foundation for how biological life has formed as we see it today. The Modern Evolutionary Synthesis is widely accepted and strongly supported by experimental and observational evidence across an array of life. Human beings have even leveraged these concepts for hundreds of years through artificial selection, imposing our own sometimes superficial selective pressures on organisms to express characteristics that we desire (such as the case of the Belgian Blue cattle, with a mutation in the myostatin gene making it a muscular, lean beef, or perhaps artificial selection in dog breeding). Richard Dawkins’ breakout book, ‘The Selfish Gene’, published in 1976, took him from an unknown voice at the University of Oxford passionate about the works of evolution across all animals, to a lauded voice in the scientific community. His concept of genes being selfish is the idea that natural selection works at the gene level, whereby genes over time become better at replication, with the organism acting as a ‘survival machine’ built to help genes propagate. It is important to note that the term ‘selfish’ is not meant metaphysically or philosophically. Figure 1 explains what ‘selfish’ means. Taking this further, it can be argued that genes helping organisms resist pathogenic attack are more likely to survive and propagate. This means the immune system does not exist to protect the body holistically but rather to protect its genes individually. The immune system evolved through the gene-centric lens As previously mentioned, the immune system has become integral to all complex organisms responding to pathogens as a selective pressure. Those genes that have conferred a greater ability to combat or resist a particular pathogen allow the organism an improved survival chance until reproductive age has been achieved. The window whereby the organism has reached reproductive maturity and is reproducing is what the genes have been selected to get, which is why many genetic pathways end up becoming detrimental to an organism in old age (explained by the antagonistic pleiotropy hypothesis- APT- and the disposable soma theory). This remains especially true for the immune system. One must also understand that only vertebrates are biologically equipped with an adaptive immune system (allowing for memory and effective response to previous pathogens), with Figure 2 explaining this difference. This supports that the immune system is a ‘selfish system’, as while many organisms survive without adaptive immunity, more complex organisms have evolved to include it because of our prolonged individual survival and delay in reproductive maturity (indicating that survivability until our reproductive window is an intense selective pressure). Immune imperfection through the ‘Selfish System’ lens We now understand there is a compelling point to be made that the immune system has evolved with the reproductive window in mind and to allow as much gene propagation in a population as possible. If we accept this point of view, it explains many of the trade-offs and imperfections of the immune system when we look at the potential harm caused by immunity. Allergies are one such example, whereby hypersensitivity causes an immune response to harmless substances, which, through the gene-centric lens, may have evolved to detect pathogens such as parasites. This further supports the ‘selfish system’ idea as reproductive success on a population scale is not impaired by a significant amount by allergies. One such study showed that women with allergies and asthma, despite having systemic inflammation, did not have a reduced fertility rate when analysing the relationship between an increase in allergic diseases in the 20 th century and a decrease in fertility globally. Chronic inflammation through persistent immune activation in old age (a concept termed inflammaging) is another such example. We previously mentioned that past reproductive age natural selection weakens, meaning that our genes are selected for early life immune optimisation, even if that means they cause problems later in old age. Processes such as cellular senescence, inflammasome activation, oxidative stress, immune cell dysregulation and so on begin to occur, leading to an increased risk of age-related diseases such as cardiovascular disease, cancer, dementia, sarcopenia and so on. Immune evolution is therefore a ‘selfish system’ because it seems to care more about gene propagation in the young to middle-aged years in comparison to long-term organism health, as many immune systems rapidly decline and become detrimental. Conclusion This perspective of the immune system as a ‘selfish system’ allows us to understand that it is not a protector of the organism throughout its life span, as we may perceive it to be, but rather that it is a mechanism evolved and optimised to propagate genetic material during the organism’s reproductive window (expanding beyond humans). This analysis of the immune system through Richard Dawkins' lens of the “selfish gene” helps us to understand many of the limitations of the immune system. Working on treatments to preserve and maintain the immune system’s healthy state, which reflects young adult life, appears to be a promising approach for future clinical prevention plans for old age diseases. There are many currently being researched and emerging treatments with this principle in mind, such as senotherapeutics and mTOR inhibitors (such as rapamycin and other rapalogs), making this an interesting field to keep up to date with. Written by Yaseen Ahmad Related articles: Darwin and Galápagos Tortoises / The genetics of ageing and longevity Project Gallery

Peruse through the current treatment discoveries for one of the deadliest diseases in the world. Learn about the factors that cause tumour growth, metastatic processes and blastomas. Cancer Articles Peruse through the current treatment discoveries for one of the deadliest diseases in the world. Learn about the factors that cause tumour growth, metastatic processes and blastomas. You may also like: Biology, Medicine Arginine and tumour growth Another breakthrough in cancer research Unveiling the cancer magnet Stem cells in vertebral bones can act like cancer magnets for spinal tumour metastasis Brain metastasis in cognitive impairment Researchers used machine learning to investigate this Novel neuroblastoma driver Uncovering the role of IGF2BP1 in neuroblastoma and its potential as a therapeutic target Previous

Delving into the 'Nudge' effect by Thaler and Sunstein Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Libertarian Paternalism and the ‘Nudge’ Approach Last updated: 02/07/26, 21:08 Published: 06/11/25, 08:00 Delving into the 'Nudge' effect by Thaler and Sunstein This is article no. 4 in a series on behavioural economics. Next article: Effect of time (coming soon). Previous article- Loss aversion . So far in our series of behavioural economics, we have discussed why and how people may make less favourable decisions than traditional economics assumes. We have spoken about how people can still be honest even when they are faced with a decision where they can be materially better off; and when someone loses their wallet, they feel more distaste than finding some money on the street; and how an endowment adds a bizarre sense of additional worth, that would cause you to think twice about trading it for something equally valuable. In today’s article, we are going to address why this is important to policy makers, and subsequently you and I, by exploring how governments and institutions can influence our decisions in ways that may seem paternalistic yet still respect individual freedom. This idea lies at the heart of libertarian paternalism . The idea behind the “Nudge” Nudge is a book written by Nobel Prize–winning economist Richard Thaler and legal scholar Cass Sunstein. Building on their 2003 paper, the book develops the idea that people’s choices can be shaped not only by the options available, but also by the context in which those options are presented — even by factors that seem trivial or irrelevant. This is where the concept of a “nudge” comes in: small design changes that steer people toward better decisions without restricting their freedom to choose. A simple change: the pension example A classic example comes from workplace pensions. Before 2008, when someone joined a new company, they were asked whether they wanted to join the company pension scheme. Most people didn’t — they took their full pay instead and failed to save for retirement. This created a growing problem for the government: an ageing population without enough savings to maintain a comfortable lifestyle. The solution was remarkably simple. Instead of asking employees to opt in to a pension, companies began enrolling them automatically, giving them the option to opt out instead. The choice remained exactly the same, pension or no pension, but the framing made all the difference. Opting out felt like losing something, and because people are naturally loss-averse, far fewer did so. In 2012, just under 50% of employees in the private sector had a pension. By 2018, after the introduction of auto-enrolment, that number had risen to around 80%. All from a change in default wording on a form. Libertarian Paternalism – a justification Paternalism is generally considered the situation where the government interferes in our choices, for better or for worse, much like a parent telling their children what they can and cannot do. In many cases, society accepts paternalism as necessary: we ban harmful drugs, make theft illegal, and impose safety regulations. But should governments really be meddling with our personal financial decisions? Should they be influencing our choices about pensions, spending, or saving? Whether they should or shouldn’t is ultimately a political question, not an economic one. However, what we can do is consider Richard Thaler and Cass Sunstein’s explanation of why policies such as pension defaults represent something fundamentally different. When the government restricts drugs or criminalises theft, it removes our freedom to choose — these are examples of hard paternalism, enforced by law. But with pensions, the government doesn’t force participation. The choice remains entirely yours: you can stay enrolled or opt out. This preservation of choice embodies the libertarian element — the freedom to decide for oneself. At the same time, by changing how the choice is presented, such as making enrolment the default option, policymakers can dramatically alter behaviour in a direction they consider beneficial. That is where the paternalistic element comes in. According to Thaler and Sunstein, this combination of freedom and gentle guidance is what defines libertarian paternalism . In Thaler and Sunstein’s eyes, nudging individuals towards better decisions through the use of policy is better and less controversial than implementing outright bans and mandates. It respects our autonomy while encouraging outcomes that they believe will improve collective welfare. If the government genuinely believes certain decisions are in the public’s best interest, then libertarian paternalism provides a way to influence behaviour without infringing on people’s right to choose. A question of freedom I do, however, pose some questions to you. If the government can influence your decision making through manipulating people’s psychology, can it truly be called libertarian ? And more fundamentally - does the government really know best? In recent years, the 'Nudge' approach has faced criticism, particularly regarding the assumptions it makes about what constitutes a “better” decision and who gets to define it. Despite this, the research continues to shape public policy across the world — from pensions and health to energy use and education. What’s crucial is that we remain aware of the ways our choices can be influenced. Recognising these nudges allows us to make decisions that best reflect our own values, circumstances, and goals. And on a deeper level, if every choice we make can be subtly shaped by those in power, how do we ensure that nudges serve the public interest — and not the interest of those who nudge? Written by George Chant Related article: The halo effect Project Gallery

Mutations in collagen and related proteins are the primary cause of EDS Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link From genes to joints: how Ehlers-Danlos Syndrome is shaped by genetics 12/09/25, 12:12 Last updated: Published: 08/11/24, 11:40 Mutations in collagen and related proteins are the primary cause of EDS This is article no. 10 in a series on rare diseases. Next article: CEDS- a break in cell death . Previous article: Breaking down Tay-Sachs . Ehlers-Danlos Syndrome (EDS) is a group of 13 inherited disorders that affect connective tissues, particularly collagen. Collagen is a crucial protein in the body that provides structure and strength to skin, joints, and blood vessels. Mutations in collagen or collagen-modifying proteins are the primary cause of the types of EDS. EDS manifests through a range of symptoms that vary significantly depending on the specific type of EDS. However, there are common symptoms that many individuals with EDS experience, particularly related to joint and skin issues. For instance, joints can move beyond the normal range, leading to frequent dislocations and subluxations, also called joint hypermobility. Additionally, the skin can be stretched more than usual, which creates a soft and velvety appearance known as skin hyperextensibility. As mentioned in Figure 1 , skin bruising, scarring and tearing are common symptoms, leading to individuals often experiencing chronic pain. Life expectancy for individuals with EDS varies depending on the type of disorder an individual has. This is due to how specific forms can have structural changes in organs and tissues, which can lead to serious life-threatening complications. For example, vascular EDS (vEDS) is associated with a significantly reduced life expectancy due to the risk of spontaneous rupture of major blood vessels, intestines, and other hollow organs. Most other forms of EDS, such as classical EDS (cEDS), hypermobile EDS (hEDS), and kyphoscoliotic EDS (kEDS), generally do not significantly affect life expectancy. However, the health complications that patients have can substantially impact their quality of life. Genetic basis As stated, the various types of EDS encompass many genetic defects, for example, cEDS is linked to mutations in the COL5A1 or COL5A2 genes, which encode the α1 and α2 chains of type V collagen. Following an autosomal dominant inheritance pattern, 50% of cEDS diagnoses inherit the condition from an affected parent, while the other half from a new (de novo) pathogenic variant. Diagnosing EDS encompasses a variety of methods. Firstly, differential diagnosis may be used to distinguish between subtypes like cEDS and hEDS by evaluating clinical features such as the presence of joint hypermobility, skin characteristics, and scarring patterns. Clinicians use these specific symptoms along with family history to differentiate between the subtypes since some, like hEDS, lack identified genetic markers, making this clinical assessment essential for accurate diagnosis and management. This process helps exclude other conditions and accurately identify the EDS subtype. Also, suggestive clinical features identifying pathogenic or likely pathogenic variants in the COL5A1 or COL5A2 genes can be done through molecular genetic testing. This testing can be approached in two ways: targeted multigene panels, which focus on specific genes like COL5A1 and COL5A2 . Alternatively, comprehensive genomic testing, such as exome or genome sequencing, does not require preselecting specific genes and is useful when the clinical presentation overlaps with other inherited disorders. Mutations in COL5A1 and COL5A2 can include missense, nonsense, splice site variants, or small insertions and deletions, all of which impair the function of type V collagen. Missense mutations result in the substitution of one amino acid for another, disrupting the collagen triple helix structure and affecting its stability and function. On the other hand, nonsense mutations lead to a premature stop codon, producing a truncated and usually non-functional protein. Splice site mutations interfere with the normal splicing of pre-mRNA, resulting in aberrant proteins. These mutations in COL5A1 and COL5A2 lead to the characteristic features of cEDS, such as highly elastic skin and joint hypermobility. Furthermore, different types of EDS are caused by specific genetic mutations, each affecting collagen in distinct ways and necessitating varied treatment approaches. VEDS is caused by mutations in the COL3A1 gene, which affects type III collagen and leads to fragile blood vessels and a higher risk of organ rupture. kEDS results from mutations in the PLOD1 or FKBP14 genes, impacting collagen cross-linking, and presents with severe scoliosis and muscle hypotonia. Arthrochalasia EDS (aEDS), due to mutations in the COL1A1 or COL1A2 genes that affect type I collagen, features severe joint hypermobility and congenital hip dislocation. Dermatosparaxis EDS (dEDS) is caused by mutations in the ADAMTS2 gene, which is crucial for processing type I collagen, leading to extremely fragile skin and severe bruising. Each type of EDS highlights the critical role of specific genetic mutations in the structural integrity and function of collagen, which consequently influences treatment approaches. Treatment Treatments for EDS primarily focus on managing symptoms and preventing complications due to the underlying genetic defects affecting collagen. Pain relief through nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and sometimes opioids is common, addressing chronic pain related to joint and muscle issues. Moreover, physical therapy may help strengthen muscles around hypermobile joints, reducing the risk of dislocations and improving stability. Orthopaedic interventions, such as braces and orthotics, are also used to support joint function, and surgery may be considered in severe cases. Cardiovascular care is crucial, especially for vEDS, involving regular monitoring with imaging techniques to detect arterial problems early. Preventive vascular surgery might be necessary to repair aneurysms or other vascular defects. Wound care includes using specialised dressings to handle fragile skin and prevent extensive scarring, relevant to mutations in genes like COL5A1 and COL5A2 in classical EDS. Understanding the specific genetic mutations helps tailor these treatments to address the particular collagen-related defects and associated complications in different EDS types. Moreover, clinical trials for treating EDS have shown both positive and negative results. For example, trials investigating the efficacy of physical therapy in strengthening muscles around hypermobile joints have shown positive outcomes in reducing joint instability and improving function. On the other hand, trials aiming to directly modify the underlying genetic defects in collagen production have faced significant challenges. Gene therapy approaches and other experimental treatments targeting specific mutations, such as those in COL5A1 or COL3A1 genes, have shown limited success and faced hurdles in achieving sufficient therapeutic benefit without adverse effects. This is evident as in mouse models the deletion of COL3A1 resulted in aortic and gastrointestinal rupture meaning that simply restoring one functional copy may not be sufficient to prevent the disease. Moreover, the unknown and partial success in identifying mutations responsible for all EDS cases has further bolstered the struggle for researchers to establish comprehensive treatment strategies. In vEDS, as it is a dominantly inherited disorder, adding a healthy copy of the gene (a common strategy in gene therapy) is ineffective because the defective gene still produces harmful proteins. Research has highlighted, however, that the combination of RNAi-mediated mutant allele-specific gene silencing and transcriptional activation of a normal allele could help as a promising strategy for vascular Ehlers-Danlos Syndrome. In the experiment, researchers used small interfering RNA (siRNA) to selectively reduce the mutant COL3A1 mRNA levels by up to 80%, while simultaneously using lysyl oxidase (LOX) to boost the expression of the normal COL3A1 gene. This dual approach successfully increased the levels of functional COL3A1 mRNA in patient cells, suggesting a potential therapeutic strategy for this condition. Conclusion In conclusion, EDS represents a diverse group of inherited connective tissue disorders, primarily caused by mutations in collagen or collagen-modifying proteins. These genetic defects result in a wide range of symptoms, including joint hypermobility, skin hyperextensibility, and vascular complications, which vary significantly across the 13 different types of EDS. Diagnosing and treating EDS is complex and largely dependent on the specific genetic mutations involved. While current treatments mainly focus on managing symptoms and preventing complications, advances in genetic research, such as RNAi-mediated gene silencing and transcriptional activation, show promise for more targeted therapies, especially for severe forms like vascular EDS. However, challenges remain in developing comprehensive and effective treatments, underscoring the need for ongoing research and personalised medical approaches to improve the quality of life for individuals with EDS. Written by Imron Shah Related articles: Hypermobility spectrum disorders / Therapy for skin disease REFERENCES Malfait, F., Wenstrup, R.J. and De Paepe, A. (2010). Clinical and genetic aspects of Ehlers-Danlos syndrome, classic type. Genetics in Medicine, 12(10), pp.597–605. doi: https://doi.org/10.1097/gim.0b013e3181eed412 . Miklovic, T. and Sieg, V.C. (2023). Ehlers Danlos Syndrome. [online] PubMed. Available at: https://www.ncbi.nlm.nih.gov/books/NBK549814/ . Sobey, G. (2014). Ehlers–Danlos syndrome – a commonly misunderstood group of conditions. Clinical Medicine, [online] 14(4), pp.432–436. doi: https://doi.org/10.7861/clinmedicine.14-4-432 . Watanabe, A., Wada, T., Tei, K., Hata, R., Fukushima, Y. and Shimada, T. (2005). 618. A Novel Gene Therapy Strategy for Vascular Ehlers-Danlos Syndrome by the Combination with RNAi Mediated Inhibition of a Mutant Allele and Transcriptional Activation of a Normal Allele. Molecular Therapy, [online] 11, p.S240. doi: https://doi.org/10.1016/j.ymthe.2005.07.158 . FURTHER READING The Ehlers-Danlos Society - A global organisation dedicated to supporting individuals with EDS and raising awareness about the condition by providing extensive information on the different types of EDS, updates on research, and resources for patients https://www.ehlers-danlos.com/ PubMed - For those interested in academic research, articles and studies on EDS. https://www.ncbi.nlm.nih.gov/pmc/?term=ehlers-danlos+syndrome Cleveland Clinic – A clinic with an extensive health library providing easy to understand and informative information about the syndrome. https://my.clevelandclinic.org/health/diseases/17813-ehlers-danlos-syndrome Project Gallery