At every stage of our lives, we think we know ourselves, or we are convinced we do.
In elementary school, you are convinced you should be a firefighter, a police officer, a pilot, or perhaps a doctor. In secondary school or high school, our headstrong teen hormones tell us we have got it all figured out.
In all honesty, I have never known myself as well as I do since I started writing. Every time I write, my thoughts, assumptions, and perspectives are challenged, bringing me closer to what matters most to me.
The gastrointestinal system is among the most intricate systems in the human body. It not only digests food and absorbs nutrients but also houses a significant portion of the immune system, coordinates complex networks of nerves and muscles, and acts as a barrier against the external environment. When problems arise, their effects can be wide-ranging. Rare gastrointestinal diseases can affect any part of this complex system and may result from various causes. Some are genetic or immune, while others result from infections, structural abnormalities, or nerve and muscle disorders within the digestive tract. Although each condition may affect only a small number of individuals, these diseases highlight the many ways the gastrointestinal system can malfunction.
The variety of rare gastrointestinal diseases becomes especially evident when examining specific cases. Very-early-onset inflammatory bowel disease, for instance, can result from genetic defects that impair immune function, causing severe intestinal inflammation at a very young age. Eosinophilic gastroenteritis is marked by an abnormal buildup of eosinophils, a type of immune cell, within the digestive tract. Intestinal lymphangiectasia, or Waldmann disease, has a structural cause, where abnormalities in the intestinal lymphatic vessels lead to leaks of proteins and other vital substances into the gut. Whipple’s disease stems from infection with the bacterium Tropheryma whipplei, while chronic intestinal pseudo-obstruction arises due to nerve or muscle issues that hinder the movement of contents through the digestive system.
Treatment varies with the cause. Immune-mediated conditions like early-onset inflammatory bowel disease and eosinophilic gastroenteritis may be treated with anti-inflammatory or immunosuppressive drugs, with some benefiting from targeted therapies. Intestinal lymphangiectasia is managed through diet and nutrition, while Whipple’s disease requires antibiotics. Chronic intestinal pseudo-obstruction might need motility medications and nutritional support, with severe cases needing intensive care. Treatments may target causes or focus on symptom control, complication prevention, and maintaining nutrition and quality of life.
The future of treatment will likely depend more on precision medicine, with improved genetic testing helping identify causes of some rare gastrointestinal diseases, especially those linked to immune system defects. This could enable treatments to go beyond managing inflammation or symptoms and target specific disease pathways. Biological therapies may more precisely influence immune activity, while advances in gene and cell treatments could offer new options for genetically defined conditions. Research into the microbiome, intestinal barrier, immune system, and neuromuscular control may also reveal new therapies. Ultimately, progress may come from understanding each condition’s specific mechanism.
Early diagnosis and access to specialised care are crucial for rare gastrointestinal diseases, which often mimic common disorders, leading to diagnosis delays. Increased awareness, better testing, specialist referral, nutritional support, and suitable treatments can make a big difference. These five diseases illustrate that rare gastrointestinal disorders are diverse, with unique causes, challenges, and treatment options. Recognising their differences is key to improving future care. Rare gastrointestinal diseases are increasingly moving from broad symptom management toward mechanism-based treatment.
A healthy immune system is surprisingly intelligent. It must identify threats, respond swiftly, eliminate dangers, and then deactivate. At the same time, it must distinguish healthy body tissues from harmful agents and retain memory to respond faster in future encounters. If any of these functions malfunction, the immune system can overreact, respond excessively or for too long, or fail to defend the body adequately. In rare immunological diseases, the immune system can attack healthy cells, trigger inflammation, damage organs through abnormal repair mechanisms, or fail to provide the protection the body needs. These disorders are highly diverse, which is one reason they are so difficult to diagnose and treat. Some stem from excessive immune activity, while others result from immune deficiency. Some primarily affect one organ, while others can involve the entire body.
The following five diseases show the variety of immune malfunction. Warm autoimmune haemolytic anaemia (wAIHA) involves antibodies destroying red blood cells and affects about 17 cases per 100,000 people in Denmark (2015). Systemic sclerosis (scleroderma) combines immune dysfunction with vascular injury and fibrosis, causing abnormal collagen in skin and organs. Sjögren’s disease primarily affects tear and saliva glands but can impact joints, lungs, kidneys, and nervous tissue. Immune-mediated necrotising myopathy (IMNM) targets skeletal muscles, leading to weakness and fibre destruction, often with antibodies against HMGCR or SRP. Conversely, idiopathic CD4 lymphocytopenia (ICL) results in low CD4 T-cell levels, increasing infection risk. These conditions show the immune system’s broad range of malfunction.
Existing medicines manage these diseases effectively, but most treatments focus on controlling symptoms of immune dysfunction rather than addressing the root cause. In wAIHA, corticosteroids are a mainstay, with rituximab, splenectomy, and other immunosuppressants used if the disease persists or recurs. For systemic sclerosis, treatment varies by affected organs and aims to relieve symptoms, prevent complications, and slow disease progression. However, there is currently no cure. Sjögren’s disease management is similar, depending on organ involvement, utilising artificial tears and saliva substitutes for dryness, and employing drugs like corticosteroids, antimalarials, or immunomodulators for systemic symptoms often off-label. IMNM typically requires aggressive immunosuppressive therapy, usually combining corticosteroids with intravenous immunoglobulin or steroid-sparing agents, and some patients need rituximab or multiple therapies simultaneously. ICL presents a unique challenge because no disease-correcting treatment is available. Care mainly focuses on preventing and treating opportunistic infections, with experimental approaches to increase CD4 counts.
Future developments aim to shift from broad immune suppression to targeting specific disease mechanisms. Researchers focus on precise targets like antibodies, cytokine pathways, and B-cell signalling. For example, wAIHA has a growing pipeline of therapies targeting complement and immune response components. Sjögren’s disease shows rapid progress, with phase 3 trials of ianalumab demonstrating positive results in 2025. Efforts also continue to refine treatments for diseases like IMNM, where current therapies rely on immunosuppressants rather than specific solutions. The goal is to move beyond broad immune suppression to identify and target the specific immune malfunction.
For rare immunological diseases, actions depend on whether the immune system attacks the body or fails to protect it. In warm autoimmune haemolytic anaemia, prompt evaluation and treatment to stop red blood cell destruction are crucial to prevent complications. Regular monitoring is vital in systemic sclerosis and Sjögren’s disease, as organ involvement may develop even with mild initial symptoms. Patients with immune-mediated necrotising myopathy need early specialist care and rehab to reduce muscle damage. For idiopathic CD4 lymphocytopenia, preventing and quickly treating opportunistic infections is key, often requiring expert advice on prophylaxis, vaccinations, and infection monitoring. Overall, immune therapy is not one-size-fits-all. Management should be tailored based on disease mechanisms, affected organs, and immunosuppression risks. The best approach includes accurate diagnosis, referral to experienced clinicians in rare immune conditions, regular complication assessments, and exploring clinical trials.
My dear, responsible readers, I know I missed the rare May and July. My apologies for the delay. I hope to catch up with you soon in the next rare post.
Rare skeletal diseases, or skeletal dysplasias, are a highly varied group of genetic and metabolic disorders that impact bone formation, remodelling, mineralisation, and connective tissue health. Even though each condition is rare individually, they collectively include hundreds of different disorders with serious clinical effects, such as severe deformities, chronic pain, increasing disability, and early death. Recent advances in molecular genetics over the last twenty years have shown that these conditions are not just different versions of a single issue but stem from distinct biological failures within the skeletal system. Consequently, rare skeletal diseases offer valuable insight into the mechanisms behind human bone development and maintenance.
Five disorders exemplify distinctly different underlying mechanisms. Fibrodysplasia Ossificans Progressiva (FOP) features abnormal BMP activation due to ACVR1 mutations, leading to progressive ossification of soft tissues. Osteogenesis Imperfecta (OI) mainly results from mutations in type I collagen, leading to fragile bones with compromised structural integrity. Cleidocranial Dysplasia (CCD) is caused by mutations in the RUNX2 transcription factor, impairing osteoblast formation and skeletal development. Hypophosphatasia (HPP) involves a deficiency of tissue-nonspecific alkaline phosphatase, leading to inadequate mineralisation due to pyrophosphate accumulation. Camurati-Engelmann Disease (CED) is driven by dysregulated TGF-β signalling, leading to abnormal thickening of the cortical bone. These diseases highlight how issues in signalling pathways, extracellular matrix, development, enzyme activity, and bone remodelling can independently lead to severe skeletal disorders.
Existing treatment strategies generally target specific diseases and are often only partly effective. Managing FOP mainly involves avoiding trauma and controlling inflammatory flare-ups, with experimental therapies targeting Activin A and ACVR1 signalling currently under active research. OI is typically managed with bisphosphonates to reduce fracture risk, in combination with orthopaedic stabilisation and physical therapy. In CCD, treatments are mostly surgical and dental, focusing on correcting craniofacial and orthodontic issues. HPP has seen notable progress thanks to enzyme replacement therapy with asfotase alfa, which greatly enhances mineralisation and survival rates in severe pediatric cases. CED poses more challenges, and current treatments include corticosteroids, pain relievers, and limited immunomodulatory options to help reduce pain and inflammation.
Future therapies are shifting from supportive care to targeted molecular interventions. In FOP, therapies targeting Activin A and BMP signalling are in advanced trials. In 2025, garetosmab, a monoclonal antibody, reduced the incidence of new heterotopic ossification lesions by over 90% in Phase III trials. Palovarotene, a retinoic acid receptor-γ agonist, became the first approved disease-modifying therapy for FOP in some countries, marking a milestone. In OI, the anti-sclerostin antibody setrusumab recently demonstrated strong improvements in bone mineral density in Phase III trials, though translating that into a clear reduction in clinical fracture rates remains an ongoing hurdle. Though CRISPR-based mutation correction remains experimental, advances in gene editing and RNA therapeutics suggest mutation-specific treatments may become viable within the next decade. Overall, this progress signals a shift from symptom management to biologically targeted and potentially preventive therapies for rare skeletal diseases.
Rare auditory diseases are a fascinating yet often overlooked aspect of hearing and balance challenges. Unlike more common issues caused by ageing or loud noise, these conditions often stem from unusual anatomical differences, immune system problems, or neural processing issues. Because they are so rare, diagnosis can be delayed, and finding the right treatment may be challenging. However, studying these rare disorders offers us invaluable insights into how our auditory system works, both in health and in illness. They are especially important because they span multiple fields, including mechanical, neurological, and immunological, highlighting the truly interdisciplinary nature of otology and neurotology.
A comparison of five rare conditions reveals their diversity. In Superior Semicircular Canal Dehiscence Syndrome (SSCDS), an additional pathway within the bony labyrinth alters inner-ear fluid movement. Acoustic energy is diverted through the dehiscent canal, reducing cochlear stimulation and heightening vestibular sensitivity to sound and pressure (Tullio phenomenon). This causes decreased vestibular-evoked myogenic potential thresholds and hearing loss resembling conductive hearing loss, despite normal middle ear function. In contrast, Auditory Neuropathy Spectrum Disorder (ANSD) involves dyssynchrony of auditory nerve firing. Outer hair cell function is usually normal, shown by normal otoacoustic emissions, but impairments in inner hair cell transmission or nerve integrity disrupt temporal coding. This leads to poor speech perception, especially in noise, due to deficits in phase locking and neural timing, rather than in audibility. The lesion may affect synapses or nerve fibres, reflecting heterogeneity within the diagnosis. Autoimmune Inner Ear Disease (AIED) and Susac syndrome both involve immune-mediated damage but differ in scope. AIED primarily affects the inner ear, whereas Susac syndrome is a systemic microvascular condition that affects the brain and eyes. AIED involves autoreactive antibodies or T-cell responses targeting inner-ear antigens, causing inflammation and fluctuating hearing loss, usually localised, though the antigens have not been fully identified. Susac syndrome involves endotheliopathy in precapillary arterioles, causing microinfarctions in the cochlea, retina, and CNS due to immune-mediated occlusion. Histology shows basement membrane thickening and endothelial damage, leading to ischemic injury rather than a direct autoimmune attack. Otosclerosis involves abnormal bone remodelling of the otic capsule, causing the stapes footplate to fixate at the oval window and block sound transmission. Sometimes, it spreads to the cochlear endosteum, adding a sensorineural component due to toxic byproducts or direct cochlear involvement. These distinctions highlight why rare auditory diseases cannot be grouped together. Each demands specific diagnostic strategies and clinical approaches.
Treatment options for these conditions vary widely depending on their underlying causes. SSCDS can often be treated surgically by addressing the affected canal, usually with good results. ANSD is more challenging to manage, with options ranging from hearing aids to cochlear implants, depending on severity and neural health. AIED is one of the few reversible causes of hearing loss and is often treatable with corticosteroids or other immunosuppressive drugs if caught early. Susac syndrome requires aggressive systemic immunotherapy, such as steroids, intravenous immunoglobulins, or biologic agents, to prevent lasting damage to multiple organs. Otosclerosis is typically managed with hearing aids or surgically via stapedotomy, which improves sound conduction by replacing the immobilised stapes. These treatment approaches demonstrate the importance of tailoring strategies not only to symptoms but also to the specific pathology involved.
Advances in precision medicine and regenerative therapies are broadening treatment options. Gene therapy and molecular interventions could correct deep-seated neural signalling mechanisms, particularly in conditions such as ANSD. Immunomodulatory treatments are also becoming more targeted, promising safer and more effective ways to manage conditions such as AIED and Susac syndrome. In addition, advances in biomaterials and minimally invasive surgery are likely to improve outcomes for structural conditions such as SSCDS and otosclerosis. Ongoing research into hair cell regeneration and neural repair has the potential to revolutionise how we treat many auditory diseases, moving from merely managing symptoms to restoring hearing function.
Fostering collaboration among audiologists, neurologists, immunologists, and ENT specialists is among the most effective strategies for improving care for this diverse set of diseases. While breakthroughs in regenerative and precision medicine are still emerging, practical efforts should focus on early intervention. Clinicians should prioritise early referral to specialist otology or neurotology centres, particularly for unusual or severe symptoms such as SSCDS or ANSD. Comprehensive testing, including advanced audiometry, imaging, and immune evaluations, is essential to identify underlying causes, such as autoimmune, vascular, or structural issues. Early targeted treatments, such as immunosuppressive therapy in autoimmune cases, can significantly improve outcomes. Audiological rehabilitation, such as hearing aids, cochlear implants, or vestibular therapy, should be initiated at the appropriate time, even while diagnoses are being confirmed.
Breslin, N.K., Varadarajan, V.V., Sobel, E.S. and Haberman, R.S., 2020. Autoimmune inner ear disease: A systematic review of management. Laryngoscope investigative otolaryngology, 5(6), pp.1217-1226. Pereira, S., Vieira, B., Maio, T., Moreira, J. and Sampaio, F., 2020. Susac’s syndrome: an updated review. Neuro-ophthalmology, 44(6), pp.355-360. Rudic, M., Keogh, I., Wagner, R., Wilkinson, E., Kiros, N., Ferrary, E., Sterkers, O., Grayeli, A.B., Zarkovic, K. and Zarkovic, N., 2015. The pathophysiology of otosclerosis: review of current research. Hearing research, 330, pp.51-56. Saidia, A.R., Ruel, J., Bahloul, A., Chaix, B., Venail, F. and Wang, J., 2023. Current advances in gene therapies of genetic auditory neuropathy spectrum disorder. Journal of Clinical Medicine, 12(3), p.738. De Siati, R.D., Rosenzweig, F., Gersdorff, G., Gregoire, A., Rombaux, P. and Deggouj, N., 2020. Auditory neuropathy spectrum disorders: from diagnosis to treatment: literature review and case reports. Journal of clinical medicine, 9(4), p.1074. Tavazzani, E., Spaiardi, P., Contini, D., Sancini, G., Russo, G. and Masetto, S., 2024. Precision medicine: A new era for inner ear diseases. Frontiers in Pharmacology, 15, p.1328460. Ward, B.K., Carey, J.P. and Minor, L.B., 2017. Superior canal dehiscence syndrome: lessons from the first 20 years. Frontiers in neurology, 8, p.177.
When life gives you lemons, you squeeze the vitamin C out of them. Yes, that is correct. Did you know that one lemon provides nearly 50% of the recommended daily intake for adults? Did you also know that citrus fibre can lower bad cholesterol, LDL, by preventing the intestines from absorbing it? That sounds like great advice. Only I do not believe in good advice. Nor do I believe in bad advice. Am I stubborn? Possibly. I believe one should evaluate one’s values and decide whether to take advice. If you live your life to meet others’ expectations, you are not living the life you want. You would be living the life others laid out for you.
My mother came from a small fishing village. One day, her brother came home with poor grades, yet again. My grandfather said something interesting. He said, ‘It is okay. If school does not work out, you just go fish’. Funny enough, one of my uncle’s friends did become a fisherman. And guess what? After 20 years, fishermen were among the wealthiest men in the village.
To be honest, most people in school or at work are not high performers. However, I do not believe in bad performers. I believe that under the right conditions, many people could be classified as high performers, whether within that system or through a journey of self-discovery. I think everyone has innate abilities that have yet to be uncovered.
I went from being an A student to a C student, then to a B student. When I was a C student, my teachers thought I was hopeless. My mum told me something interesting. She said I needed someone to teach me how to learn because the way I was learning was not working. Little did she realise that the standard educational system was not working. It never did.
I do not believe in good or bad advice. I believe in science and values. The average lemon contains 30 to 50 mg of Vitamin C. That is a fact. Whether you should squeeze it into your water is a matter of personal choice. We are told that only 10% of us are high performers. The fishermen were low performers in a classroom, but they were the wealthiest men in the village once they got on a boat. So, who is the low performer now?
Do you know how I went from a C to a B student? I sat at the back of the lecture hall doing newspaper puzzles instead of sitting in the front row to pretend I enjoyed boring lectures. Do not take this the wrong way, I have met teachers so good that the entire class passed. I moved back up to a B, not because I worked harder but because I stopped trying to fit the standard mould and started using my innate abilities, even if they looked like a Sunday crossword puzzle.
In reality, most people just follow the stepping stones. Then reality slaps you in the face. The standard system is not working because it tries to turn every lemon into the same lemonade. If you are a C student, you may not be hopeless. Maybe you are just a fisherman sitting in a math class.
The power law beats the bell curve, Yours Possibly
Did you know that studies estimate nearly 80% of all toys end up in landfills, incinerators, or the ocean, unrecycled? No? Me neither. A UK study showed that the average child owns around 493 toys throughout their childhood, which could fill over 34 wheelie bins of clutter. Furthermore, research indicates that doubling the lifespan of toys through reuse, material recovery, or on-demand production could reduce greenhouse gas emissions per toy by 30-50% by preventing repeated manufacturing cycles. Recycling plastic toys into new printable material has been shown to lower emissions by 3-4 kg of CO₂ per kilogram of plastic compared to using virgin material.
What if we could do that? I would like to call it The Imaginarium. Instead of fitting toy creation into a standard household printer, imagine a specialised device dedicated solely to play. This toy printer would not compete with other tools or furniture. It would integrate more naturally into the child’s environment, both physically and conceptually. Its goal is not efficiency but inspiration. This device produces toys on demand: a rattle for a toddler, a puzzle for a rainy day, or a moving creature for a brief fascination. When the toy is no longer needed, it can be returned to the device, disassembled, and recycled. The toy disappears, but the materials are (mostly) conserved.
The Imaginarium uses various material cartridges, each tailored for a specific type of interaction. Soft toys are crafted from flexible, foam-like materials that resemble plush, making them lightweight, durable, and easy to clean. For infants, some options could include natural, non-toxic substances derived from sources such as cellulose, starches, or algae, which are already utilised in biomedical and food-safe applications. There are even toys that might be edible, eliminating risks during early play. Structural toys like blocks, puzzles, and simple tools are made from durable, baby-safe plastics. While these materials are not edible, they can be fully recycled within the device. They feature precise, snap-fit connections and can be reused multiple times without degradation. More advanced toys often combine printed shells with embedded movement or lighting features, all while avoiding the inclusion of delicate electronics in the manufacturing process.
Movement and interaction rely not on disposable batteries but on a limited number of reusable energy cores. These sealed units are shared among toys and enjoyed repeatedly over many years. Each core contains a solid-state power source with simple actuation or lighting components, all fully enclosed and certified as safe for children. The toy printer does not generate energy. Instead, it beautifully prints objects around these cores, gently embedding them into secure shapes that cannot be easily removed or misused. When a toy is no longer needed, simply return the core to the system to recharge and reuse in new designs. This means a household can get by with just a few energy cores, sharing them across many different toys rather than owning dozens of battery-powered ones.
Much of this system already exists in parts. Recyclable, self-healing polymers are currently under active research. Bio-based, food-safe printable materials are used in medical and laboratory environments. Modular electronics, sealed power units, inductive charging, and digital toy design are all well-established technologies. What still needs to be developed is their integration into a closed domestic cycle that considers toys as temporary expressions rather than permanent possessions.
The challenges are mainly cultural and regulatory. Safety certification must evolve to accommodate reconfigurable objects. Standards are needed for material purity, reuse cycles, and embedded energy modules. Parents would need to trust systems instead of objects. The issue of design also arises. Toys are not neutral; they embody values, behaviours, and stories. Bringing toy manufacturing into the home also transfers responsibility.
Today, toy manufacturing emphasises scale over durability. Items are mass-produced, shipped globally, used briefly, and discarded. In contrast, a domestic toy printer shifts this approach by producing fewer items, reducing shipments, and decreasing plastic waste. Producing toys only as needed and recycling materials and energy afterwards helps reduce waste at both the product level and throughout supply chains. This approach reduces transportation, lowering CO₂ emissions, and reduces manufacturing, resulting in less raw material extraction.
With The Imaginarium, toys are not everlasting. The materials are. Power is. Design is. Play is.
Once upon a time, very close by, there lived a very beautiful leech called Bureaucracy….
I remember a story a friend of mine told me. A person was walking his dog in the park. Then the small dog decided to go down into the rabbit hole. Literally. After that, the fire brigade had to come and locate the little dog in the rabbit hole. A few things came to mind. Among them were “oh what a stupid dog” and “oh what kind of an idiot walks a dumb dog without a leash (yes, I am a cat person, but do not worry, I also love smart dogs). But perhaps the most important thought was “Did I just pay 35% income tax for that?”. Now, that is what I call a waste of tax money.
Unfortunately, humans resemble that small dog much more than we like to admit. We enjoy sending people down rabbit holes, and if we fail, we end up going down them ourselves. Yes, I mean bureaucracy.
Bureaucracy is the human tendency to create rabbit holes, label them carefully, assign someone to guard the entrance, and then act surprised when people fall into them. It thrives on good intentions and consumes time, energy, and common sense. Much like a leech, it does not attack aggressively. It attaches quietly, almost elegantly, and before you notice, you are weaker, slower, and inexplicably tired.
At first, it seems harmless. A form here. A signature there. “Just one more document,” it softly whispers. And because it presents itself as order, safety, and responsibility, we seldom question it. After all, who could oppose procedure? Fairness? Doing things “the right way”? But somewhere between form number three and form number seventeen, something curious occurs. The process becomes more significant than the outcome. The rules outlast their purpose. The leech grows fat.
And when things inevitably go wrong, as they always do, we respond in the only way we seem to know: by sending more people into the hole. Committees are formed. Departments are consulted. Firefighters arrive, funded by that same 35% income tax, to rescue a problem which did not need to exist in the first place.
The tragedy is not the existence of bureaucracy. Some organisation is essential. The real tragedy is that we mistake complexity for intelligence and procedure for wisdom. Like the small dog, we keep rushing ahead, convinced that someone else has checked if the hole is safe.
And this is where the leech shows its true talent.
Bureaucracy does not appear as a monster. It is refined. Symmetrical. Adorned with courteous language and official stamps. It reassures you that everything is under control while quietly consuming. It does not drain blood in a single violent moment. It sips over minutes, hours, years. A meeting here. A delay there. A requirement no one recalls inventing.
Like any clever leech, it convinces the host that its presence is essential. “Without me there would be chaos,” it claims. And so we allow it to remain. We even admire it. We call it “institutional knowledge.” We create flowcharts and display them on walls.
Meanwhile, the dog remains in the hole.
By the time we realise how much has been taken from us. Time, money, patience, initiative. We are already too exhausted to remove the leech. Doing so would require a form, possibly two, and certainly a committee. And so the leech remains, beautiful and well-fed, while we argue over who should recognise that we are bleeding.
Bureaucracy does not solve problems. It feeds on them.
Once upon a time, very close by, there lived a very beautiful leech called Bureaucracy.
And it is still there.
And it lives inefficiently ever after, Yours Possibly
Cancer is often characterised by uncontrolled growth, but ultra-rare cancers adhere to entirely different biological principles. Some are driven by a single fusion protein that modifies the epigenetic landscape, while others originate from immune precursors circulating in the bloodstream. Certain types excel by hijacking kinase signalling in otherwise healthy organs, whereas others survive within the protected environment of the brain. Rare cancers are not merely infrequent variants of common tumours. They are mechanistically distinct entities that challenge our understanding of how malignancy begins, progresses, and responds to treatment.
The range of rare cancers is striking. NUT Carcinoma (NC) results from a fusion that disrupts differentiation through epigenetic reprogramming, leading to an aggressive carcinoma. Alveolar Soft Part Sarcoma (ASPS), originating from mesenchymal tissue, features a fusion that promotes angiogenesis and early metastasis despite slow primary growth. Blastic Plasmacytoid Dendritic Cell Neoplasm (BPDCN) is not a solid tumour but a malignancy of innate immune precursors, often initially appearing in the skin before spreading systemically. Fibrolamellar Hepatocellular Carcinoma (FL-HCC) affects young people without liver disease and is driven by a kinase fusion protein. Primary Central Nervous System Lymphoma (PCNSL) occurs within the immune-privileged brain, where both biology and treatment are limited. These cancers demonstrate that rare cancers are a spectrum of distinct mechanisms, tissues, and challenges.
Treatment strategies reflect this biological diversity. Aggressive multimodal therapy, combining surgery, chemotherapy, and radiation, is often used for NC, but outcomes remain poor. ASPS responds poorly to standard chemotherapy but may respond to VEGF inhibitors, which block new blood vessel growth that is essential for tumour expansion. For BPDCN, CD123-targeted therapies like tagraxofusp, delivering a cytotoxin to malignant cells, have transformed treatment, signalling a move toward lineage-specific immunotherapy. Managed primarily by surgery when possible, FL-HCC benefits most from complete tumour removal, as systemic therapies often have limited success. PCNSL requires high-dose methotrexate (HD-MTX) to cross the blood–brain barrier and target CNS lymphoma cells, sometimes followed by autologous stem cell transplantation (ASCT), where a patient’s own stem cells are reinfused after intensive chemo to restore bone marrow. Across these diseases, precision medicine is vital, with understanding driver mutations or cellular origins guiding therapy.
Future treatments rely on more targeted biological approaches. BET inhibitors are small molecules that disrupt abnormal chromatin-binding proteins that sustain oncogenic transcription and are being studied for NC to reverse differentiation blockade. In ASPS, immune checkpoint inhibitors (ICIs), which counteract inhibitory signals on T cells to boost anti-tumour immunity, are under investigation given the tumour’s immunogenic nature. For BPDCN, chimeric antigen receptor T-cell therapy (CAR-T), where a patient’s T cells are engineered to target CD123-expressing cancer cells, shows promise as a future treatment. In FL-HCC, research centres on selective PKA pathway inhibitors to block continuous kinase signalling driven by the fusion protein. Additionally, new CNS-penetrant targeted therapies specifically designed to cross the blood–brain barrier, alongside combination immunomodulatory treatments, could transform PCNSL therapy. Rare cancers often act as models of clarity, as their dependence on a single fusion or pathway makes them highly suitable for precise targeted treatment.
Early molecular testing is essential for both patients and clinicians today. Rare cancers often go misdiagnosed or are mistaken for more common types, leading to treatment delays. Referring patients to specialised centres, enrolling them in rare cancer registries, and exploring clinical trials can significantly improve outcomes. Many ultra-rare cancers, such as NC, ASPS, BPDCN, FL-HCC, and PCNSL, have specific molecular drivers or biological contexts, making comprehensive genomic profiling urgent rather than optional. Despite their rarity, these cancers demand exceptional accuracy. Understanding their biological uniqueness is the crucial first step towards effective treatment.
Have you ever signed up for a service or content that includes the word “professional” somewhere? And then immediately regretted it? After several attempts to unsubscribe, you just ended up blocking this flood of unwanted content. Welcome to the club!
I understand the importance of marketing. At the same time, I can decide for myself what I want, and I really do not need a commercial or an email to tell me. If you grew up watching “normal” TV, you probably remember your life was filled with commercials. However, you might recall that some commercials were really fun to watch, and you did not mind rewatching them a few times. Just maybe not five times during one movie.
On the other hand, you have probably also seen or heard commercials that irritate you so much that it annoys you when you see the brand, and it makes you never want to buy from them in the first place.
Then there are types of marketing that deserve a special place in hell. They use extortion, like dramatically longer delivery times if you do not become a member. But you know what? If I really need it, I would just buy it from another retailer. And yes, that other retailer might actually make more money on that specific product because you paid a little more. But you know what? That retailer earned it by not being annoying.
The real difference between a nuisance and a brand leader lies in shifting from interruption to invitation. Effective marketing, like Toyota’s “Today, Tomorrow, Toyota” or the recent “Let’s Go Places,” works because it creates a consistent promise rather than just making noise. It respects the “Value Exchange,” the unspoken agreement that if a brand takes 30 seconds of your time, it should give you something in return, whether that’s a laugh, a useful insight, or a solution to a real problem. Poor marketing fails because it focuses on message volume instead of how quickly it delivers value. When a brand emphasises short-term metrics, like email open rates, over building long-term trust, it risks losing its reputation for a quick click.
This frustration underscores the delicate balance between effective communication and digital noise. Usually, the main factors are Permission, Signal, and Equity. Great marketing follows Seth Godin’s idea of “Permission Marketing,” where content is so well-targeted that recipients want to receive it instead of seeing it as spam. It is about maintaining a high “Signal-to-Noise” ratio and standing out by solving a real problem you face, rather than just shouting into the void. Companies using “special place in hell” tactics, often focus on immediate “Direct Response” sales at the cost of their “Brand Equity.” While they might make a quick sale today, they risk losing long-term trust and goodwill that could lead to repeat business.
Ultimately, the best marketing does not feel like a sales pitch. It feels like a well-timed recommendation from a friend who genuinely understands what you like.
To special places in hell, Yours Possibly
Further Reading
Aaker, D.A. (1991)Managing Brand Equity: Capitalizing on the Value of a Brand Name. New York: Free Press. Binet, L. and Field, P. (2013)The Long and the Short of It: Balancing Short and Long-Term Marketing Strategies. London: IPA. Cialdini, R.B. (2007) Influence: The Psychology of Persuasion. Rev. edn. New York: Harper Business. Godin, S. (1999)Permission Marketing: Turning Strangers into Friends and Friends into Customers. New York: Simon & Schuster. Godin, S. (2018)This Is Marketing: You Can’t Be Seen Until You Learn to See. New York: Portfolio/Penguin. Newport, C. (2016)Deep Work: Rules for Focused Success in a Distracted World. New York: Grand Central Publishing. Sharp, B. (2010) How Brands Grow: What Marketers Don’t Know. Melbourne: Oxford University Press. Simon, H.A. (1971) ‘Designing Organizations for an Information-Rich World’, in Greenberger, M. (ed.) Computers, Communications, and the Public Interest. Baltimore: Johns Hopkins University Press, pp. 37–72. Searls, D. (2012)The Intention Economy: When Customers Take Charge. Boston: Harvard Business Review Press.
Why are women so often portrayed as evil? Because they are not. Period.
I am not a feminist in the ideological sense. I believe in equality for everyone, regardless of their gender or sexuality. But I grew up with a grandfather who was unusually progressive for his time. He used to say: if all women wore trousers, there would be nowhere left in this world for men to stand.
He was not insulting women. He was recognising power.
Women are depicted as evil, dirty, or dangerous, not due to weakness, but because men have always known two things at once: that women are essential and that they cannot be completely controlled. This mix of dependence and fear has never led to generous storytelling.
This logic still holds today. When a woman slacks off at work, people are more likely to hire men afterwards, but when a man slacks off, we simply hire another bloke because this one will be different. How exactly does this logic work?
The same pattern extends upwards. Chaotic world politics is not just about geopolitics. It is a massive pecking order, governed by the same dominance logic that influences gender, labour, and power at all levels of society.
Throughout history and across different cultures, a common pattern endures: women are frequently blamed when things go wrong. Eve ate the forbidden fruit. Pandora released the contents of the jar. The witch prepared her potion. The shapeshifter altered her form. These tales are ancient, sacred to some, well-known to many, and deeply ingrained in societal explanations of themselves.
They did not occur by chance.
Historically, men held authority over storytelling. Myths, laws, and sacred writings emerged as societies aimed to impose order on a world riddled with uncertainty. Forces like fertility, birth, blood, sexuality, death, and transformation were unpredictable and uncontrollable. Women personified these forces. They experienced bodily changes, bleeding, and birth. Positioned at the cusp between beginnings and endings, between ongoing continuity and sudden rupture, their power was both majestic and unsettling.
Anthropologist Mary Douglas suggested that societies tend to classify things they cannot easily control as dangerous. In rigid systems, ambiguity is viewed as a threat. Women, inherently associated with ambiguity, often symbolise it. As a result, many narratives portray change as feminine and blame it accordingly.
Eve’s curiosity led to knowledge and exile, while Pandora’s curiosity caused suffering to spread. Both myths originated in societies that reinforced patriarchy, inheritance, and male lineage. Psychologist Erich Neumann referred to this as a cultural fear of the “Great Mother” archetype: the feminine as both creator and destroyer. Rather than accepting this complexity, these cultures portrayed feminine power as dangerous, tempting, or flawed.
This pattern appears in folklore, where women are more inclined than men to shapeshift into animals such as spiders, snakes, birds, or cats. These creatures are associated with the night, weaving, poison, and liminal spaces. Weaving was traditionally a woman’s task: storytelling became a tangible craft, with fate woven by hand. The spider symbolises both creator and trap, while shapeshifters represent survivors and threats. Silvia Federici notes that women known for knowledge, healing, midwifery, herbalism, and oral tradition were demonised during social change. Uncontrollable phenomena became sources of fear.
Psychologically, this phenomenon is projection. Historically, men exercised external power through law, force, and authority, while women wielded symbolic power associated with desire, life, and continuity. Societies projected fears such as chaos, mortality, temptation, and curiosity onto women and punished them through stories. This explains why women are often portrayed as temptresses, corruptors, or transformers, symbolising instability.
This pattern is not universal. When women share stories, interpretations evolve. In matrilineal or egalitarian cultures, women act as guides, teachers, and creators. Spider women craft worlds, and shapeshifting goddesses are playful, wise, and protective. Demonisation increases when male-dominated religious or political institutions formalise these stories, transforming oral traditions into a fixed canon.
These stories remain relevant because myths continue to shape perceptions, roles, and judgments today. Despite striving for equality in laws, work, and visibility, old blame narratives persist, depicting women as too curious, ambitious, disruptive, or excessive.
Modern retellings of ancient tales.
Questioning these myths does not undermine belief but explores the fears and significance behind them. The woman might not have been the actual issue, but a symbol of change, which always threatens those who want to maintain the status quo.
Do you know what I find fascinating about scammers? They are incredibly creative. From the weirdest porn fetishes you did not know even existed to the most useless products, making you wonder if they have ever worked in pornography, telemarketing, or infomercials. It is the most beautiful love-hate relationship. The most ridiculous email that makes you laugh so hard you fall out of your chair, to heartbreaking news you read online that makes you wish you were an octopus so you could strangle eight scammers at once.
Language was once a key sign of fraud, with poor grammar, awkward phrasing, and spelling mistakes revealing it. However, this defence is weakening, especially in English. Since English is best understood by AI, it is more difficult to detect scams in English. Most language models are trained on English data, enabling them to produce fluent, idiomatic, and contextually suitable text. Tasks that once needed skilled scammers can now be done quickly, at scale, and at low cost. As a result, linguistic mistakes that once helped identify scams are becoming less common, removing an important safeguard.
This shift is crucial because English dominates global business, technology, finance, and online platforms. It is the most adaptable language for fraud, reaching the broadest audience. AI removes language barriers, so polished English no longer indicates legitimacy but access to better tools. This is evident in corporate scams, where phishing emails now mimic a professional tone, hierarchy, and timing, sounding calm and courteous and blending into routine communication.
This development may heighten vulnerability among younger users, as AI removes linguistic cues that signal legitimacy. Younger users trust polished, correct language online, and AI can provide it, boosting trust rather than suspicion.
Tone introduces risk. AI not only corrects grammar but also enhances politeness, confidence, and emotional stability. Scams no longer rely on urgency or aggression. They can be patient and helpful. In English, politeness conveys authority, reducing suspicion even with unusual requests, creating a false sense of security. Users were advised to watch for spelling and grammar errors as fraud signs, but AI has rendered this advice obsolete. Now, clean language signals automation, not legitimacy. The real risk is that scams become harder to distinguish from genuine communication.
Since language often does not reveal scammers, detection depends on behaviour and context. It is not about how messages sound but rather what they request, the pressure they apply, and breaches of norms. Future scam awareness should focus on recognising manipulation patterns rather than just poor English, and should be implemented soon in all official languages.
AI rapidly reduces the gap that once kept users safe, with English at its centre. When scams appear more professional and less suspicious, the danger of fraud rises, and confidence in false sources increases.
In our comfortable modern world, scammers keep our fight-or-flight response active. I doubt they will ever stop, so we should use these experiences to strengthen our awareness.
The devil is no longer in the spelling and grammar. It is in your gut.
Humans have always been drawn to spectacle. Drama. Competition. Entertainment. The blood that once stained the Colosseum has now been replaced by dollar signs. Just when 2025 seemed uneventful, Netflix, Paramount Skydance, and Warner Bros. delivered a finale with more zeros than we can count.
Yes. We love entertainment. And I do value copyright protection and proper business deals. They safeguard creativity and sustain industries. Yet, even with these truths, a question that has long remained unspoken is starting to surface. What are we even talking about?
Instead, we allow the blood to evaporate in the sun. Because life can be cruel. Because many of us are too busy carrying our own burdens to notice what is drying up around us. After a stressful day, all we want is to sit down, relax, enjoy, and fall asleep. And somewhere between exhaustion and entertainment, real human suffering continues silently in the background.
While corporations trade IP at a price tag hefty enough to rival the GDP of entire nations, millions of people still struggle for clean water, food, and safety. Beyond spectacles, there is a world full of genuine human stakes. It makes you question where our true priorities lie.
We know the price of everything and the value of nothing.
Spectacles change, human needs remain, Yours Possibly
We shifted from an efficient home office to a more socially hybrid arrangement, and now we are somehow almost back to being completely brain-dead on-site. And I thought “light bulb”? Nope. What I really thought was Bruce Willis’ Surrogate? How about you?
If you have seen that film, you might recall that the ending was quite lively. But fear thee not. It resonates with us because we already dedicate parts of our lives to remote activities. We shop, work, and even consult doctors via video calls. So, why do we need exobots? Consider an ambulance caught in traffic. Paramedics can stabilise the patient, but what if a trauma surgeon could virtually assist via a robot while the patient is still en route? In disaster zones, a structural engineer could assess and shore up unstable buildings without personal risk. In infectious disease wards, doctors could examine patients physically without exposure. In an increasingly volatile and fast-paced landscape, the gap between science fiction and real-world needs is closing.
The underlying technology for this vision is already in its early stages and advancing quickly. Tele-surgery, where surgeons operate robotic tools remotely, is no longer just theoretical. The first full remote operation occurred in 2001 during the Lindbergh procedure, with a surgeon in New York performing surgery on a patient in France via fibre-optic connection and robotic systems. More recent procedures have connected surgeons and patients over tens of thousands of kilometres, managing latency effectively, including bariatric surgeries between France and India and experimental use of 5G networks to cut control delays. Hospitals have also performed robotic surgeries, such as hernia repairs, from hundreds of kilometres away. These developments are enabled by teleoperation systems that translate a human operator’s movements into robotic actions using high-fidelity control interfaces, stereoscopic vision for depth perception, and haptic/force feedback for tactile sensation. Ongoing research aims to further improve these systems through advanced leader-follower configurations and predictive control algorithms to ensure smooth, secure remote interactions, even in the presence of packet delays or losses.
Nevertheless, real-world exobots face substantial obstacles before they can become broadly feasible. Communication systems must deliver ultra-low, predictable latency, usually under a few tens of milliseconds for precise motor control, often requiring dedicated infrastructure beyond standard internet or 5G. Highly dexterous robotic manipulators capable of mimicking human hand function across various tissues and forces are still under development. Current remote surgeries are limited by imperfect haptic feedback, which can affect how surgeons apply force. Issues such as power supply, sterilisation, redundancy, sensor fusion for stable telepresence, and safety certification raise costs and complexity. Additionally, legal liabilities, jurisdictional credentialing, cybersecurity, and ethical concerns for remote interventions remain unresolved. These challenges are not insurmountable, but they explain why remote surgical teleoperation remains mostly at pilot or specialised stages rather than widespread emergency use, and why future exobots will need advancements in networking, robotics, medicine, and regulation to effectively manage emergency situations.
From the earliest moments of life, minor developmental errors can cause significant and lasting impacts. Rare congenital diseases are conditions present at birth resulting from disruptions during embryonic or foetal development. Unlike genetic rare diseases, which primarily result from DNA mutations, congenital disorders may originate from a combination of genetic, environmental, or unknown factors, often presenting as structural malformations, metabolic imbalances, or developmental delays. Recognising congenital diseases as a distinct category allows healthcare professionals and families to prioritise early diagnosis, prompt interventions, and personalised management plans.
The spectrum of rare congenital diseases is extensive. Congenital Diaphragmatic Hernia (CDH) involves a structural defect in the diaphragm that allows abdominal organs to enter the chest cavity and impairs lung development. Tetralogy of Fallot combines four heart defects, leading to cyanosis and circulatory issues, and is often associated with chromosomal deletions, such as 22q11.2. Congenital Hyperinsulinism (CHI) results from mutations that disrupt pancreatic beta-cell function, leading to ongoing hypoglycaemia and risk of neurological damage. Merosin-deficient Congenital Muscular Dystrophy (MCMD) stems from defective muscle proteins, weakening skeletal muscles, and sometimes impacting the brain. Lastly, Congenital Hypothyroidism can be caused by thyroid dysgenesis or biosynthesis defects, which delay growth and cognitive development if left untreated. These diseases highlight that congenital conditions can be structural, metabolic, muscular, or endocrine, underscoring the importance of developmental processes in early life.
Current treatments for rare congenital diseases are usually tailored to each condition and are mainly supportive, focusing on managing complications and improving quality of life. For example, CDH is typically repaired surgically shortly after birth, along with vigilant neonatal respiratory support. Tetralogy of Fallot often requires early corrective heart surgery, sometimes in multiple stages. CHI is treated with medications like diazoxide that inhibit insulin secretion, and in severe cases, partial pancreatectomy. MCMD depends on physiotherapy, orthopaedic support, and respiratory care, as there is no cure. Congenital Hypothyroidism has a notably effective treatment. Early thyroid hormone replacement to prevent growth delays and cognitive impairment. In all these cases, early diagnosis and coordinated care are essential, as prompt intervention can significantly improve outcomes, even without cures.
The management of congenital rare diseases is becoming increasingly personalised and promising. For CDH, advancements in foetal surgery and prenatal imaging may enable corrections before birth, thereby improving lung development and survival rates. Tetralogy of Fallot could benefit from minimally invasive surgeries and tissue-engineered heart patches, reducing the need for multiple procedures. In CHI, new gene-targeted therapies and pharmacological chaperones might address the underlying beta-cell defects instead of merely managing symptoms. MCMD is a promising candidate for gene therapy, exon skipping, or stem cell–based regenerative treatments aimed at restoring muscle function. Finally, for Congenital Hypothyroidism, although hormone replacement is effective, early intervention could be enhanced through genetic screening and prenatal diagnosis, helping to prevent disease effects before birth. Overall, advances in molecular medicine, prenatal diagnostics, and regenerative technologies point to a future in which congenital diseases are addressed at their developmental origins rather than solely managed after birth.
Managing rare congenital diseases requires a synergy of early detection and a coordinated, multidisciplinary approach. Modern newborn screening and advanced prenatal diagnostics, such as those for Congenital Hypothyroidism, create a “window of opportunity” for intervention before irreversible damage occurs. However, technology alone is not enough. The key element is the “medical home” model. This approach unites neonatologists, surgeons, geneticists, and therapists into a single team, shifting care from merely treating symptoms to supporting the whole child. Ultimately, combining genetic and developmental information enables clinicians to move beyond generic protocols, creating personalized treatment plans that not only improve health outcomes but also give families hope for their child’s future.
From day one, the future takes shape, Yours Possibly
Psychological research increasingly indicates that seeking meaning leads to more enduring well-being than simply chasing happiness. A sense of purpose in life offers us resilience, direction, and perseverance. While pursuing long-term happiness can sometimes lead to unhappiness, this is known as the paradox of happiness. Nonetheless, I cannot help but notice how naturally joyful babies are. So, when does that happiness begin to fade?
Babies are almost always happy, except when nature calls. Unless they are experiencing some kind of distress like hunger, pain, illness, diaper emergency, or not enough cuddling, babies are genuinely joyful.
Perhaps happiness does not fade because life worsens, but because our awareness burdens us more. As we age, we accumulate memories, expectations, and comparisons. These may help us navigate life, but can also diminish our joy. For some, this heightened consciousness appears early, even before adulthood has a chance to smooth out those rough edges.
How can we regain happiness without chasing it? Research indicates that happiness often returns when we live with purpose. Purpose shifts our focus outward. Contributing, accepting responsibility, and finding meaning beyond ourselves lessen self-criticism. Although purpose does not eliminate suffering, it provides context, fostering a more peaceful and enduring happiness.
I usually appreciate change because I think that without it, nothing evolves and progress stalls. The real questions are: what exactly constitutes a change? When do changes bring benefits? When are they detrimental? When are they simply unnecessary? And do we truly need to change at all?
Not everything needs constant modification. Often, resistance can serve as a valuable asset. If everyone were easily swayed, the world would be in chaos. Thus, it takes as much determination to initiate change as to stay steady.
Change is more than just movement. It is a purposeful transformation. Like a butterfly, not every stage is visible or glamorous. There is the egg, quiet and unremarkable. The caterpillar, ravenous and restless. And the chrysalis, which seems lifeless. From the outside, nothing seems to happen, but internally, everything is being broken down and rebuilt. Change often appears as stagnation before taking flight. We usually see the cocoon as an ending, but in reality, it is a period of negotiation between what was and what could be.
Every stage of the butterfly’s development serves a purpose. The caterpillar does not rush its hunger. Instead, it must eat, grow, and understand its body’s limits before it can even imagine having wings. The chrysalis is not merely a break but a process of refinement. Old parts dissolve to make way for stronger ones. When the butterfly finally emerges, it is not just changed, but fully prepared. Its gains in one stage lay the groundwork for the next. Without the patience involved in growth and the silent discipline of transformation, flight would be impossible.
So, what defines a change? It might not be the act of becoming different, but the willingness to be undone. Good change broadens us. It sharpens our vision, deepens our empathy, and enables us to act with greater purpose. Bad change, however, fractures without rebuilding. It is movement driven by fear rather than purpose, alteration for the sake of escape. Some changes are unnecessary, like tearing open a cocoon before the wings have developed. Interruption masquerading as progress.
Do we really need to change? Not necessarily. Roots are as important as wings. The tree does not envy the butterfly, nor does the butterfly regret being a caterpillar. Growth requires both progress and patience, understanding when to adapt and when to remain steadfast. When chosen intentionally, resistance is not stagnation but a form of stability. An affirmation that not everything delicate needs altering, and not everything complete requires fixing.
This balance embodies wisdom. Knowing when to shed skin or stand firm, and honouring change as a deliberate, necessary act. It is earned and irreversible, like metamorphosis.
Genetic rare diseases form a unique and often misunderstood group within rare medicine. Unlike disorders limited to a single organ system, these diseases originate at the molecular level, in DNA itself. They can affect nearly any tissue in the body. A single gene mutation may disrupt development, metabolism, neurological function, or cellular maintenance, sometimes all at once. This fundamental overlap explains why rare genetic diseases often defy traditional medical classifications yet share common diagnostic and therapeutic challenges. Recognising these conditions as a category helps patients, families, and clinicians focus on the root causes rather than just the symptoms.
The diversity within this category is remarkable. Fibrodysplasia Ossificans Progressiva (FOP) is caused by a signalling mutation that transforms soft tissue into bone. Hutchinson–Gilford Progeria Syndrome (HGPS) results from a defect in nuclear structure that accelerates ageing. Congenital Insensitivity to Pain with Anhidrosis (CIPA) arises from the failure of sensory neurons to develop, leaving patients unable to feel pain or regulate temperature. Alkaptonuria is a metabolic disorder caused by an enzyme deficiency, which leads to pigment accumulation in connective tissues. Finally, Fatal Familial Insomnia (FFI) is driven by toxic protein misfolding in the brain. These diseases are rarely clinically similar, yet all stem from specific genetic errors, emphasising the central role of DNA in rare diseases and highlighting the wide range of mechanisms that genetics can disrupt.
Current treatments are mostly supportive and vary greatly. FOPrequires careful handling of trauma and pain, but no cure exists. HGPSpatients benefit from cardiovascular and growth-focused care. CIPA care concentrates on preventing injuries and overheating. Alkaptonuria can be managed through dietary restrictions and symptom relief, while FFI has no effective therapy beyond palliative care. Overall, most interventions target complications rather than fixing the underlying genetic defect. This variability reflects both the complexity of human genetics and the historical limitations of medicine in addressing DNA-level disorders.
Genetic rare diseases are at the forefront of medical innovation. Gene therapy and gene editing offer the potential to correct or compensate for defective genes. RNA-based drugs may silence harmful mutations or restore missing proteins. Advances in genomic sequencing, early diagnosis, and personalised medicine are paving the way for treatments that could slow or even prevent disease progression at a molecular level. Although most of these therapies are still experimental, they represent a fundamental shift from symptom management towards directly addressing the root causes.
For patients and families today, the most immediate opportunities lie in personalised medicine. Genetic testing can identify the specific mutation causing a disorder, enabling treatments to be customised to an individual’s molecular profile. Clinical trials increasingly focus on specific gene variants, providing access to therapies tailored to a patient’s unique genetic makeup. Multidisciplinary care remains vital, but the combination of early diagnosis, detailed genetic information, and emerging targeted therapies is already improving outcomes. By understanding rare genetic diseases at the molecular level, patients and clinicians can make informed, proactive decisions that translate personalised medicine into practical strategies today.
It is easy to blame our disappointments on big, disruptive events like pandemics, elections, or natural disasters. After all, they did fuck up our lives. But what they truly reveal is who we really are, both as individuals and collectively. They dismantle our routines, assumptions, and excuses. Pressure reveals the remnants of resilience, fear, courage, and doubt.
When the world collapses, some hands open, others form fists. Crisis cuts through the noise and lays instincts bare. Stress causes us to cling to our identities and beliefs. Lines turn to stone. Words lose their beat. Polarisation intensifies. Fear takes the stage. Freedom is taken hostage.
A crisis is a black hole moment, a point of no return. Once you pass the event horizon, everything is stripped away. The singularity reveals only the truth. Crisis does not create monsters. It frees them.
While I enjoy discussing eccentric future technological ideas, it is equally important to examine the other side of the coin. To be clear, this piece aims to be a statement rather than a provocation. The typical hierarchy reveals two things. First, there is someone at the very top of the food chain. And second, there is a massive, broad base that supports everyone else.
Africa provides the raw materials that enable our high-tech world, yet the continent receives only a small share of the value. Cobalt is essential for nearly every smartphone and electric vehicle battery. The Democratic Republic of Congo holds about 70% of the world’s reserves but gains only 1–3% of the total global value chain. The same applies to coltan, lithium, and platinum group metals. Africa supplies the foundation, but most of the wealth from refining, processing, and manufacturing flows abroad.
The imbalance for other commodities is equally striking. Cocoa and coffee create global markets worth tens of billions each year, yet less than 10% of the final value remains in the producing countries. Gold, diamonds, and platinum often see only 10–15% of their market value stay on the continent, despite these resources being crucial to the luxury, industrial, and electronics sectors.
Suppose Africa claims a share based on contribution and necessity, considering environmental costs, labour, and global reliance on its resources. In that case, estimates indicate it could control 15–20% of the value chain for high-tech metals and 20–30% for essential agricultural commodities. This is roughly five to ten times what is currently realised, translating into billions of dollars annually that could fund education, infrastructure, and technological development across the continent.
The figures reveal more than just economics. They shed light on the hidden cost of progress. Every device, every battery, every screen that fuels the dreams of the future carries an unseen debt. A wealth quietly extracted from African soil, labour, and potential. And within this lies the quiet revolution waiting to emerge: the shift from extraction to empowerment.
The hidden cost of the future is not unavoidable. It becomes apparent when we follow the flow of materials and wealth from African mines to the devices we hold in our hands. It also indicates a different kind of future. One where Africa shifts from being a supplier of raw materials to a centre of innovation and production. Local refineries, battery factories, and technology hubs could turn what is now mere extraction into lasting development.
This is not a revolution of barricades, muskets, or sudden upheaval. It is a systemic revolution: a shift in global trade, investment, and production rules that recognises Africa’s rightful stake in the technologies of tomorrow. The AfCFTA, regional industrial initiatives, and investments in local high-tech infrastructure are early sparks of this change, as they claim a fairer share of value and build the capacity to transform resources into knowledge and products.
Imagine a world where the cobalt powering a battery benefits the community that mines it, where the gold in a circuit funds schools, and where the minerals beneath African soil become the foundation for African-made innovation. This vision is ambitious but also realistic. It demands courage to overhaul systems that have long externalised costs and concentrated profits elsewhere.
The technologies we envision hold a record of human choices, values, and injustices. Recognising the hidden cost of the future is the first step towards creating a shared, equitable one that reflects the contributions of all who make it possible.
Progress without fairness is extraction, Yours Possibly
Welcome to the 2026 New Year’s resolutions! Why? Well, because we have learned from my Anti-Kairos post that we do not like change, and therefore we continue to make new New Year’s resolutions each year. And if you do not remember, because you have not read that post, then you should make it your 2026 New Year’s resolution right now and get on with it!
How many times did someone in 2025 tell you, “I am busy”? Better yet, how many times have you told someone else, “I am busy”? I have one simple solution. If it has a date, if it costs you time, if it even remotely smells like time? It must be in your calendar. Yes. Unless you have a job where everything happens on the fly and at random, you should own your calendar. In fact, the Heisenberg Uncertainty Principle was proven to be incorrect in 2025. Now, I am not a quantum physicist, but that sounds impossible. Yet, science has proven that it is possible, even in one of the most difficult subjects. Where does this leave us?
I am an agenda hedonist. And no, I do not live in my calendar. Being an agenda hedonist allows me to manage my free time. The more you plan for things that eat up your time, the more time you free up for other activities. After having many conversations with “the one who shall not be named here”, someone who has no sense of time, it made me realise something. I have been explaining it all wrong. You cannot explain time to someone who does not understand time.
Instead, I decided to use money as a metaphor. After all, time is money. I know many disagree because, unlike money, you cannot save time, but for most people, both time and money are finite. A lot of times, your pay is fixed. You can manage and budget time in similar ways to money. And yes, everything you would earn above that, extra, as a bonus, would not suit this comparison, but normally, you budget within your fixed income, including your savings. Your savings here are your free time.
Yes, yes, I can read your mind, telling me “I do not have time for this”. If emergency room doctors thought like you, we would not have emergency rooms in hospitals but many more morgues. If air traffic controllers thought like this, planes would start to drop out of the sky. ER doctors and air traffic controllers use triages to manage things that are unpredictable. Customer and IT service representatives use tickets with escalation rules to manage their numbers. If you define yourself as extremely busy, it means you need to build a resilient structure to manage your time.
First things first, the meetings you have every day should neverever be budgeted as “rent” or “mortgage”. If you do this, then you would end up homeless or paying interest instead of your principal. Your meetings should be your shopping list for the week. This means you are flexible to decide which items are important and what needs to be added last minute, and which ones can be removed from the list. Start with the basics, the stuff you will always need, like vegetables and fruits. If your shopping list feels like a holiday shopping list, then you know you have been too generous. And when it feels like you have been shopping at Prada or Versace? Well, that means you have been using credit, and that is expensive. Why? Because now you have to pay back every month, meaning, you now need to catch up with work, A LOT.
So, what should be categorised as “rent” or “mortgage”? Your core responsibilities, including deadlines, deliverables, and strategic work, should be categorised as non-negotiable. They keep you employed and trusted. Time is your payslip. Spend it like you mean it. Pay your rent or principal first, avoid living on interest, save for growth, and shop meetings wisely. If you would not bankrupt your finances, do not bankrupt your time either.
Happy New Year, Yours Possibly
An ER doctor on triaging your “crazy busy” life – Darria Long (TED)
Why Meetings Suck and How to Fix Them – Adam Grant (TED)
Earlier this year, I began this blog with The Rare Responsibility. Now, it feels only natural to conclude 2025 with some of the rare discoveries that shaped it.
At the core of that shift was Huntington’s disease. For decades, Huntington’s has been the emblem of a devastating, stubborn genetic disorder. However, in 2025, we finally obtained credible clinical and mechanistic evidence indicating that it is possible to alter the course of the disease in humans. On one hand, a gene therapy programme showed promising early-stage human data. Patients treated with a direct brain-delivered therapy displayed significantly slower progression compared to historical or matched controls. Although the cohort was small, and long-term safety and durability remain uncertain, this represents the strongest indication yet that we can modify Huntington’s in humans.
On the other hand, parallel research in cells and organoids has advanced. Scientists demonstrated refined control over the mutant huntingtin gene, proving that biology is not only targetable but also manageable. This dual confidence in clinical evidence and mechanistic understanding fundamentally transforms the field’s view of Huntington’s. From an inevitable decline to be endured, to a biological mechanism to be corrected.
Yet, Huntington’s was not the only headline. 2025 also saw the first case of personalised gene editing. A baby with carbamoyl phosphate synthetase 1 (CPS1) deficiency received a custom CRISPR‑based treatment tailored to their specific mutation. This was not part of an extensive commercial programme. In fact, it was essentially a one-patient medicine with significant implications. It demonstrated that we can move from individual genomic diagnosis to personalised genome editing, under compassionate or emergency use, and achieve meaningful clinical benefits. It is now an active, patient-centred reality.
However, before a personalised cure can be crafted, the mutation must be discovered. This brings us to the diagnostics front, where Solve-RD, a pan-European collaboration, made significant progress. By re-analysing genomic data from thousands of previously undiagnosed patients using improved pipelines and updated variant-interpretation tools, the team identified over 500 new rare disease diagnoses. This is not just an academic achievement. It highlights that a significant part of the rare disease challenge lies in diagnosis. Without knowing who has what, treatments, no matter how advanced, remain out of reach. In 2025, we recognised that diagnosing rare diseases is not limited by a lack of data, but by a lack of interpretation. And that is changing rapidly.
Alongside the progress in diagnosis and early testing, 2025 was equally significant for regulatory approvals. Approximately 14 new drugs received FDA approval, primarily for rare diseases. These included treatments for hereditary angioedema (both acute and preventive), neurofibromatosis type 1 (plexiform neurofibromas), tenosynovial giant cell tumour, diffuse midline glioma, and long-waited options for Barth syndrome, IgA nephropathy, a subset of phenylketonuria, myasthenia gravis, and haemophilia A/B. These approvals not only signify scientific progress but also demonstrate regulatory and commercial willingness to develop therapies for small patient populations.
Beneath the headlines, the clinical-trial engine itself has accelerated. According to industry intelligence, in the first half of 2025, there were around 6,071* Phase I–III interventional trial starts worldwide. Using a conservative industry estimate that roughly 35% of pipeline programmes target rare diseases, that indicates over 2,100* rare disease trials began in just six months. Extrapolating to the whole year, we are likely to see approximately 4,200* new rare disease trial starts in 2025. Meanwhile, the global number of active rare disease trials (across all phases) is likely to remain in the low tens of thousands. A remarkable scale for what was once a niche category.
This scale matters because it is not just about more trials, but about smarter ones. Gene therapy, genome editing, and RNA modalities are no longer artisanal, one-off efforts. Manufacturing and quality control are being standardised. Instead of handcrafted gene vectors or RNA molecules made patient-by-patient, we are beginning to see repeatable workflows, modular production lines, and manufacturing units that function more like foundries.
The industrial maturity brings us to a significant indicator of capital and confidence. In October 2025, Novartis announced it would acquire Avidity Biosciences for $12 billion in cash. Avidity is a pioneer in Antibody‑Oligonucleotide Conjugates (AOCs), a delivery platform designed to target RNA therapeutics directly to muscle tissue. Its pipeline includes three late-stage neuromuscular programmes: del-zota (for Duchenne muscular dystrophy), del-desiran (for myotonic dystrophy type 1), and del-brax (for facioscapulohumeral muscular dystrophy). Notably, Novartis made the deal even as Avidity spun off its early-stage precision cardiology programmes into a separate company, SpinCo, indicating that Novartis is increasing its focus on genetically defined neuromuscular diseases. The acquisition not only provides Novartis with new drug candidates but also a platform. It affirms that RNA‑delivery technology is considered sufficiently significant to justify a multi-billion-dollar purchase.
Beyond the Novartis–Avity acquisition, 2025 was a notably busy year for rare disease deals and strategic partnerships. Sanofi broadened its focus on rare immunology and precision haematology by acquiring Blueprint Medicines for several billion dollars, with Ayvakit, a systemic-mastocytosis therapy, at its core. Merck KGaA boosted its rare oncology efforts by buying SpringWorks Therapeutics, while BioMarin expanded into metabolic and genetic disorders by adding Inozyme Pharma to its portfolio. Meanwhile, Alexion, AstraZeneca’s division dedicated to rare diseases, continued to invest heavily in gene therapy platforms, acquiring next-generation AAV capsid technology to support future ultra-rare indications. Overall, these developments show that rare diseases are no longer niche markets but are now key to long-term innovation strategies in the biopharmaceutical industry.
Yet, amid all this progress, a realistic outlook persists. Not all experiments will succeed. Many early clinical results, such as the Huntington gene therapy, come from small patient groups and require long-term follow-up. Manufacturing scale is improving, but the high cost of goods remains a significant barrier to cell and gene therapies. Regulatory endpoints for very rare diseases cannot always depend on conventional large-scale clinical trials. Digital or molecular endpoints may be necessary, although these methods are still being tested and refined. While Novartis’ Avidity deal sends a strong signal, it also reveals a truth. Not all companies will take on the risk of low-volume, high-complexity manufacturing. The capital structure needed for ultra-rare therapies may differ from Big Pharma’s usual approach.
In short, 2025 marked the year when rare disease treatment stopped being an accident. It was no longer about individual, heroic founders or niche gene-therapy studios. Instead, platforms matured, capital aligned, data interpretation expanded, and regulatory systems began to adapt. The coming years will not just be about demonstrating that rare diseases are solvable. They will focus on proving that treating rare diseases is sustainable.
“Good morning, Mara. You are late.” Her ring vibrates. She rolls her eyes. “It is Christmas, not a board meeting.”
She steps out of bed. The floor feels comfy and warm. The new solar paint adjusted its absorption overnight, perfectly storing extra power for a cold morning like this one.
Next to her bed, The Loomer has her outfit ready for today. A freshly printed, red knitted-look jumpsuit. She puts her fresh clothes on.
“So soft and warm, hmmm,” she murmurs, and tosses her dirty pyjamas back in The Loomer.
In the kitchen, The Forge blinks green. She taps plate, fork, knife, and mug on the interface. In seconds, Mara removes her printed kitchen items from The Forge. She places the plate in the Edible Lab and sets it to avocado toast with bio-yeast spread. “Breakfast smells like Sunday morning,” she thinks to herself.
After breakfast, Mara returns the plate and cutlery to The Forge. The machine washes and recycles the materials, readying them for the next item.
Mara walks towards her front door. On the way, she picks up her exosuit.
“Commute mode,” she says. “Confirmed,” the suit replies, tightening around her calves.
She sprints down the frosted streets and looks at the unfinished 3D-printed homes made of non-recyclable materials as she passes. Halfway to the café, her exosuit slows and flickers red on her ring.
She taps her ring. “Nearest available pod, please. And schedule a drone recovery for my suit.”
Moments later, a self-driving pod slid to the curb, its door opening with a quiet sigh. “Good morning, Mara. Destination?” “Central Café.” “Confirmed.”
The pod glides into the flow of silent capsules, each one whispering across the city. Drones buzz sky-high throughout the city, dropping organic snowflake confetti.
At the café, she steps out to the scent of freshly printed coffee. Jin is already there, scrawling on a napkin with his smart pen.
“Still writing by hand?” she teases.
“It helps me think,” he says with a grin. “Even if the ink is virtual.”
They talk about work. The modern prostitution, as people like to call it. No one has fixed jobs anymore. Companies simply rent expertise through the global talent grid. Mara’s profile lists systems architecture and energy ethics, and this week she is working for a firm in Nairobi.
She sighs with relief. Months of cell calibration, endless data checks, and now her sister is well.
Jin smiles. “Best Christmas ever.”
After coffee, they stroll into the Old Quarter, where the city’s annual Analogue Christmas Market shimmers with lights, wooden stalls dusted with solar snow.
“Welcome to the most futuristic, yet nostalgic Christmas market,” Jin shouts.
At the first stall, a vendor demonstrates self-inflating pod lacquer. Shimmering coatings that ripple with the slightest touch.
“Inflates on collision, seals within seconds,” the saleswoman said.
Mara laughs. She still has not upgraded her own pod.
The next booth displays some gel-based nets for doors and windows. She brushes her hand through the membrane. It feels like the mango pudding she had last Monday. The net seals itself as she removes her hand.
“Keeps out pollution and bugs,” the guy winks.
“There!” Mara says as she pulls Jin across the Christmas market. The Edible Lab printer cartridges. Mara samples a Nordic Sweet Root pastry and saves the recipe instantly to her ring. She purchases the cartridge and places it in a drone to have it delivered home.
Jin points at a booth showcasing exobots. Remote-controlled robotic suits for working anywhere.
“Oh yes,” Mara says, grinning, “they have outsourced all the robot engineers to the other side of the world. Now they just use these exobots to fix toilet problems remotely. Saves a ton on travel, apparently.”
“It really smells like Christmas,” Mara says to Jin, as she looks up. Drones glint like fireflies, delivering packages to homes across the city.
That evening, Mara returns home with her hair full of drone confetti and the smell of the Christmas market. She takes her clothes and feeds them into The Loomer. A fresh pair of soft pyjamas is already waiting, printed from the fibres of the pair she tossed in this morning. She pulls on her new, warm and cosy pyjamas and smiles.
Nearby, the exosuit has returned quietly, waiting for its overnight charging cycle. Mara stores it neatly in the corner. Her ring dims the lights and sends her sister a message:
“Merry Christmas. Cannot wait to see you swimming again.”
Outside, the drones are still dropping organic snowflake confetti from the sky, and Mara thinks, “Best Christmas ever.”
Global demand for blood continues to rise, driven by ageing populations, complex surgeries, and cancer treatments. The WHO estimates that over 40 per cent of global blood donations originate from just 16 per cent of the world’s population. Regular donors are ageing, and younger generations donate less frequently. Competing demands from plasma centres increase pressure. Maintaining a motivated, voluntary donor base is becoming a significant public health challenge worldwide. Donation rates fluctuate during holidays, pandemics, and crises. In many developing countries, hospitals receive only a fraction of the blood they require each year.
Matching donor and recipient blood types involves more than just the ABO system. For people with rare phenotypes such as Rh-null or Bombay, finding a compatible donor can take weeks. Maintaining rare-donor registries and cold-chain storage is costly and logistically challenging. Every donation must be tested for transfusion-transmissible infections like HIV, hepatitis B/C, and syphilis. Low-resource regions often lack the latest screening tools, creating safety gaps. Emerging pathogens require testing protocols to adapt continuously. Blood must be collected, processed, tested, stored, and transported under strict temperature control. Power outages, transport delays, or refrigeration failures can spoil supplies. Rural and conflict-affected areas face the greatest challenges due to weak logistics. Blood components have limited shelf lives: red blood cells last 42 days, platelets 5-7 days, and plasma up to one year if frozen.
These challenges demonstrate why the ability to print blood on demand is essential. Imagine a world where hospitals can print compatible, pathogen-free blood ready for transfusion. Currently, we cannot print blood itself, but we can produce the environment and components necessary for blood to function. Researchers have already developed plasma-based 3D printable materials, often enriched with platelets, that facilitate wound healing or support cell growth. Some laboratories can produce individual plasma proteins, such as albumin or clotting factors, using recombinant techniques, but combining them into a functional, transfusable plasma remains a future objective. Blood is considerably more complex than plasma alone. It is a living suspension of plasma, red and white blood cells, and platelets. What has been printed are red blood cell models at the microscale for studying oxygen transport and vascular networks, which could one day carry synthetic or donor-based plasma.
Plasma is chemically complex, but blood is both chemically and mechanically complex. From a printing or synthetic perspective, blood is harder to replicate because it requires reproducing the plasma composition, the cellular components, and their interactions, as well as their mechanical behaviour. Lab-grown red blood cells must carry oxygen, deform properly, and survive long enough to be effective. Printed blood cells degrade more quickly than natural ones, limiting practical application. Additionally, any printed blood or plasma must be sterile and immunologically compatible.
Printing blood and plasma could transform medicine. It could eliminate shortages, provide personalised transfusions, and deliver life-saving therapies anywhere. Perhaps we do not need to print every single drop of blood? Instead of recreating every cell and protein outside the body, we could print its precursors or boosters that the body itself multiplies into functional blood. One promising approach uses hematopoietic stem cells (HSCs), the progenitors of red cells, white cells, and platelets. In the lab, these cells can be expanded into millions of functional blood cells. Imagine printing or injecting a small number of these stem cells and letting them grow into a full complement of blood components inside a bioreactor or in the patient’s own body.
Other strategies focus on oxygen carriers. Haemoglobin-based molecules and perfluorocarbon emulsions can temporarily transport oxygen without needing full red blood cells. Meanwhile, engineered platelet or plasma precursors could act as bio-boosters, stimulating the body to produce its own clotting factors and immune components. Furthermore, implantable micro-bioreactors are being researched. Tiny devices seeded with precursor cells could continuously produce blood components on demand, potentially reducing the need for donor blood entirely.
We may not need to print every drop of blood. By combining printing technology with the body’s natural biology, we can create a system where a small, engineered input multiplies into a complete, functional lifeblood.
There are two kinds of people. Those who thrive in a minimalist micro-apartment and those who can never have enough space. After all, capitalism keeps us hooked and our homes full. Yet, interior designs share one striking trait. There is no clutter. Right. Everything is perfectly tidy.
We have already explored The Loomer, which revolutionises our closets, and the Edible Lab, which transforms our kitchens. This leaves us with the remaining, miscellaneous, capitalistic clutter. What if we could replace all of that as well?
Meet The Forge, where the Greek mythological Hephaestus encounters future technology. It is the ultimate must-have household 3D printer that prints on demand. Anything you need, from cutlery to plant pots, or small decorative items, including a screwdriver or a bobby pin.
With The Forge, everything you need can be printed on demand. The reusable nanoblocks are reprocessed and ready to become something entirely new. By turning clutter into convenience and ensuring nothing goes to waste, The Forge changes how we live, consume, and create.
Beyond convenience, The Forge could fundamentally alter our perspective on products. Instead of mass-producing items and shipping them globally, manufacturers might concentrate on digital designs.
At the core of The Forge lies a groundbreaking material. Nanoblocks are modular units designed to bond at the atomic or molecular level, enabling them to be reshaped and reused endlessly. The device uses a combination of additive manufacturing and molecular assembly methods, precisely layering nanoblocks to produce objects with exact geometry, strength, and durability. Advanced AI scanning guarantees accurate reproduction of complex or flexible items such as slippers or a small screwdriver. The process also incorporates temperature and pressure regulation at the microscale, allowing for seamless bonding without damaging the nanoblocks, ensuring every print matches the strength of the original material.
Modern 3D printing has progressed beyond simple plastics. Multi-material printers can combine flexible and rigid polymers, metals, and even ceramics in a single object. Researchers are exploring self-healing polymers and recyclable printing materials, where used items can be reprocessed into new filament. Molecular assembly techniques are also developing in laboratories, enabling precise control of atomic or nanoscale building blocks, though only on a small scale so far. Nanotechnology has produced modular units capable of forming complex structures, and AI-assisted scanning can reproduce real-world objects with high fidelity. These advances suggest that a reusable, universal home printer is conceptually aligned with the ongoing trajectory of current science.
Current multi-material 3D printers and recyclable polymers still face limitations in scale, speed, and precision compared to what The Forge would demand. True nanoblock assembly at home would require breakthroughs in molecular control and bonding reliability, while ensuring the material can endure repeated reuse without deterioration. Energy efficiency and safety also present obstacles. Managing heat, pressure, or chemical processes at a microscale must be both reliable and user-friendly. Lastly, integrating AI scanning to accurately replicate a wide range of everyday objects, from flexible slippers to delicate glassware, remains in its early stages. Overcoming these challenges will require advancements in materials science, nanoscale manufacturing, and AI-driven design.
In a world where we produce more than we consume, The Forge offers more than just convenience. It provides sustainability. By printing items on demand and reusing nearly every nanoblock, we significantly cut material waste, fostering a circular economy within our homes. Less mass production lowers CO₂ emissions at the source, while fewer deliveries and store trips cut traffic-related emissions. It envisions a future where convenience, creativity, and sustainability are intertwined.
If you have ever fed a baby, you know that the baby will create the most adorable hot mess before it even takes its first bite. Each time, you try a different strategy in the hope of coming out clean, only to find that the baby has just made you and created an even cuter mess.
Adults often believe that negotiation is mainly about strategy, logic, and compromise. This just spells overcomplicated. Babies are emotionally genuine. They cry when upset and laugh when happy. Many adults think it is more professional to conceal feelings during negotiations, but research on emotional contagion shows that people respond more to authentic feelings than to scripted words. Clearly expressing your real priorities can be much more persuasive than a vague, neutral email.
Babies teach us the importance of persistence and timing. In fact, when you say no, they laugh and do it explicitly, then clap their hands. Repeated effort influences behaviour, a principle psychologists refer to as operant conditioning. Additionally, babies instinctively cry at the perfect moment when parents are most likely to respond. Adults can learn from this by observing moods, priorities, and energy levels before making a request.
Furthermore, babies do not give hints. Instead, they express exactly what they want. Loud, proud, and unmistakable. Adults benefit from clarity by framing requests simply and directly, outlining what they need, why it matters, and how it benefits everyone. Clear communication removes guesswork and leads to faster results. Moreover, a toddler might throw a tantrum and then start giggling mid-meltdown, keeping parents engaged. Adults can learn from this disarming pivot. A moment of unexpected humour or warmth can break a stalemate and remind the other party that you are all human.
Another key strategy is to attract attention through presence. Babies capture attention by being fully present. Every smile, cry, or coo is an entire performance. Adults can mirror this by engaging in active listening, asking thoughtful questions, and using attentive body language. People naturally gravitate towards those who make them feel heard and appreciated. Finally, babies remind us not to fear appearing demanding. They ask, demand, and express themselves freely, yet adults tend to cave. In adult life, confidence is convincing. Asking clearly and assertively is much more effective than overthinking politeness or worrying about seeming pushy.
Negotiating like a baby does not mean throwing tantrums or being unreasonable. It means being authentic, persistent, clear, timely, playful, present, and confident.
I have been recycling for a while now. Still, each time, I am perfectly shocked by the sheer volume of packaging that exceeds the actual waste. We produce over 400 billion kilograms (~900 billion pounds) annually. Most of this waste ends up in the environment. A major challenge is that effective waste management infrastructure requires investments, which many countries are reluctant to make. Without proper waste management, rubbish continues to flow into rivers and oceans. What if we could incentivise people to manage their own waste?
Or better yet, what if we could create a powerful incentive for one of the world’s largest industries to start collecting it? The real estate industry is among the largest sectors globally, with an estimated value of $4.13 trillion as of 2024. Meanwhile, housing prices continue to rise. Concrete, steel, and cement are costly and contribute significantly to carbon emissions. Cement alone accounts for nearly 8% of global CO₂ emissions due to the heavy process of heating limestone to produce clinker. We are surrounded by waste while millions struggle to find shelter. In India and Kenya, innovators are transforming unrecyclable plastic into furniture and paving bricks, but what if we could print houses from unrecyclable plastics? We could sell our waste to the construction industry, where it becomes a valuable commodity rather than a problem.
Different plastic materials can be combined using compatibilizers. These molecules help different plastic properties bond and act like emulsifiers by linking polymer chains to create a stable material. Shear-thinning allows the mixture of emulsified plastic to flow while maintaining its shape. This could enable us to print small, lightweight houses in the future. Engineers incorporate sand, crushed glass, or fly ash to stiffen the molten plastic. The plastic acts as an adhesive, and the particles form a skeleton. When cooled, polymer chains wrap around the grains, creating a composite stronger in compression than plastic alone. Lab studies show compressive strengths of several megapascals, suitable for walls or small buildings. Bonding between printed layers is also essential. Each new strand of plastic must stay warm enough for its polymer chains to interweave with the layer below. If it cools too quickly, the structure could separate. Furthermore, any final material must be durable. Plastics expand and contract with temperature more than concrete does, so the composite needs to withstand weathering, load-bearing stress, and fire.
Turning waste plastic into printable building material faces several challenges. Plastic waste contains many polymers with different properties. Melting them together produces unpredictable results. Compatibilizers, precise thermal control, or pre-processing to sort plastics are required. Plastic is flexible but weak under compression. Adding sand, ash, or fibres helps, but the balance is tricky. Too much filler makes it brittle, too little and the walls deform. Cooling adds complexity. Uneven cooling can cause warping or cracks. Additives and post-print heating cycles can relieve internal stress. Fire safety is also critical. Heated plastics may release toxic fumes. Safe flame retardants and filtration are necessary. Finally, building regulations are not written for plastic composites. Engineers must demonstrate strength, fire resistance, and long-term durability before people can live in these homes.
New reprocessable polymers can melt and bond repeatedly without losing strength. Incorporating them into waste streams could produce universal binders that make mixed plastics printable and durable. Nanomaterials such as nanosilica, graphene, and basalt fibres can reinforce composites, enhance strength, and boost fire and thermal resistance. Hybrid systems can combine printed plastic shells with bamboo, steel, or foamcrete cores. Plastic layers insulate and waterproof, while the inner frame supports the load. This approach makes housing cheaper, lighter, and more sustainable. If we succeed, the very material that defined our age of waste could become the foundation of our circular cities, forming the walls that shield us from storms.
Today, we can lease almost anything. Cars, phones, the internet. In Sweden, some people technically lease their homes because the principal is cheaper than rent. There are even stores that let you lease outfits for a weekend. Soon, we might not just lease miscellaneous items. We will lease human beings. Our time, our knowledge, our expertise. We will all be employed by the same shark. A global brothel that rents out human intelligence by the hour. Consulting companies started this trend decades ago, when they realised selling advice was more scalable than selling products. They just did not realise they were inventing the prototype for the labour economy of the future.
It is a dream come true. No more job hopping, messy resignations, or “What animal would you be?” interviews. Your career becomes a subscription service. Companies only pay what they need. Why carry the overhead of full-time employees when you can stream talent like a Netflix show? Experts can pick exciting projects, avoid office politics, and potentially earn more by keeping themselves in constant, well-paid motion. Some people already live like this. Think freelancers, consultants, and independent specialists.
The infrastructure for renting people already exists. AI matching systems pair specialists with projects faster than any recruiter. Remote work tools make geography irrelevant. HR algorithms predict skills demand before the company even knows it. To the system, we are just a bundle of skills. A few keywords, performance metrics, and a rating. From an economic perspective, it is efficient. Why keep experts idle when they can be continuously leased? Why build a team when you can assemble one on demand?
When the dream is over, the nightmares start creeping in. When your worth is updated in real time, your future becomes more unpredictable. When everything is rentable, we stop belonging to ourselves. In a world where expertise is rented and scarce, access does not come cheaply. It comes at auction. Companies will have to bid for top talent, and the highest bidder usually wins. Start-ups and underfunded companies might never get the experts they need, no matter how innovative or deserving they are. Meanwhile, deep-pocketed corporations will dominate the most critical skill markets, creating a winner-takes-all dynamic. While the Goliath streams the premium content, David gets the ad-filled low-resolution version.
The future of work is your profile in a basket, ready for checkout. It is not so different from what we have always done. Just upgraded with personal branding, sharper suits, and cloud-based scheduling. We are all learning to sell ourselves more elegantly.
To cheap thrills and expensive regrets, Yours Possibly
The human skin is a remarkable work of art. A single touch can trigger an adrenaline surge and make our hearts race. It acts as a knight in shining armour, shielding us from sunburn and dehydration, defending against infections, regulating temperature, and sensing the external environment. It even allows us to communicate emotions through colour changes and expressions. Conditions like acne or eczema are common and familiar, but there are rare dermatological diseases that manifest in different ways. These illnesses can result from genetic mutations, immune system malfunctions, or abnormal cellular growth. Studying them not only enhances patient care but also uncovers hidden insights into how our skin functions.
A genetic mutation causes harlequin ichthyosis and appears at birth. Newborns are encased in thick, diamond-shaped skin plates that make them highly vulnerable to dehydration and infection. In contrast, pemphigus vulgaris usually develops in adulthood, with the immune system mistakenly attacking the proteins that hold skin cells together, resulting in fragile, painful blisters. Dermatofibrosarcoma protuberans (DFSP) is a rare skin cancer that grows slowly from fibroblasts in the dermis. It rarely spreads but requires precise surgery to prevent recurrence. Netherton syndrome combines genetics and immunity, leading to scaly, fragile skin, brittle hair, and severe allergic tendencies. Finally, cutaneous T-cell lymphoma, specifically the mycosis fungoides subtype, shows how malignancy can mimic common eczema-like patches, which may progress over years into plaques, tumours, or systemic disease. These five conditions highlight the remarkable diversity of rare dermatological diseases and emphasise the importance of specialised understanding.
Treating these rare diseases varies greatly depending on their causes. Babies with Harlequin Ichthyosis require intensive care, including hydration, infection prevention, and systemic retinoids to soften their thickened skin. Pemphigus vulgaris is managed by calming the immune system, using corticosteroids, immunosuppressants, or targeted therapies like rituximab to reduce the production of harmful antibodies. DFSP depends on precise surgical removal, with drugs such as imatinib reserved for small residual tumours. Netherton Syndrome is mainly managed through supportive care, emollients, gentle skin hygiene, and emerging biologics to control severe allergies. Cutaneous T-cell Lymphoma requires a staged approach. Early stages may respond to topical treatments and phototherapy, whereas advanced cases might need systemic medications or even stem cell transplantation. Across all these conditions, early recognition and targeted treatment greatly improve outcomes.
Gene therapy and protein replacement may eventually target the underlying defects in Harlequin Ichthyosis and Netherton Syndrome, progressing beyond merely managing symptoms. Autoimmune conditions like Pemphigus Vulgaris are benefiting from new biologics that precisely modulate immune responses with fewer side effects. For cancers such as DFSP and Cutaneous T-cell Lymphoma, targeted therapies and immunotherapies are being refined to eliminate malignant cells while specifically protecting healthy tissue. Overall, research is advancing towards addressing root causes, offering the potential for longer-lasting control and, in some cases, cures.
In clinics, next-generation sequencing panels now routinely identify genetic disorders such as Harlequin Ichthyosis or Netherton Syndrome, reducing the years-long diagnostic delays faced by many families. In autoimmune conditions like Pemphigus Vulgaris, rituximab and other targeted biologics have transformed treatment, often replacing long-term steroid dependence with sustained remission. For DFSP, molecular testing for the COL1A1–PDGFB fusion not only confirms the diagnosis but also guides the use of imatinib, a precision therapy tailored to the tumour’s genetics. In Cutaneous T-cell Lymphoma, newer phototherapy regimens, interferon-based treatments, and clinical trials of checkpoint inhibitors are expanding options beyond palliative care. Meanwhile, international patient registries and skin biobank collaborations enable researchers to share genomic and clinical data, accelerating discoveries that once took decades.
