The Blog

CRISPR used to sound like one of those technologies that belonged entirely in science-fiction movies. Edit DNA? Change genes? Sounds futuristic. Except it isn't really futuristic anymore.

CRISPR-based treatments are now reaching actual patients. In 2026, the FDA expanded approval of Casgevy, a CRISPR-based treatment for sickle-cell disease, to children as young as two. Another experimental CRISPR treatment has also shown that a single infusion could keep lowering cholesterol for at least a year. Suddenly, “editing DNA” doesn't sound quite so far away.

The basic idea is surprisingly simple: find a particular piece of DNA and change it. CRISPR acts a little like a biological editing tool, allowing scientists to target specific genetic instructions.

That opens up a very different way of thinking about medicine. Instead of treating a problem again and again, could we fix the underlying genetic cause?

But once CRISPR leaves the lab, things get complicated. Scientists have to worry about unintended edits, long-term effects, how to deliver the treatment to the right cells, and whether these therapies can become affordable enough for more than a tiny group of patients. The FDA is now developing specific safety guidance for genome-editing treatments, showing just how quickly this field is moving.

And then comes the slightly uncomfortable question: if we can eventually edit genes to prevent disease, what happens when people want to edit things that aren't diseases? Where do we draw the line?

That's where CRISPR stops being just a biology story and starts becoming a much bigger conversation about medicine, ethics and what we actually want to change about ourselves.

CRISPR isn't a magical “delete anything” button, and scientists still have plenty to figure out.

But one thing is for sure: gene editing has moved from something scientists experimented with in cells to something doctors can actually use in patients.

The next chapter isn't really about whether we can edit DNA.

“It’s about figuring out when we should.”

If cells can divide to make new cells, why don't they just keep doing it forever? More cells sounds useful, right? Unfortunately, biology has a few limits built in—and those limits are actually pretty important.

One reason is telomeres. They are protective sections at the ends of our chromosomes, a bit like the plastic tips on shoelaces. Each time most cells divide, their telomeres get slightly shorter. Eventually, they become too short for the cell to keep dividing safely.

The cell may then enter senescence, meaning it stops dividing. This might sound inconvenient, but it helps prevent cells from multiplying uncontrollably.

And that's important because uncontrolled cell division is a major feature of cancer. Cancer cells can bypass some of the normal limits on growth and keep dividing when they shouldn't.

Some cells, such as certain stem cells, can divide much more often because they can maintain their telomeres using an enzyme called telomerase. Interestingly, many cancer cells also use telomerase to help them keep dividing.

So cells aren't meant to divide forever. Their limits are actually part of the body's safety system.

“Basically, your cells have a biological speed limit—and ignoring it can cause some very serious problems.”

There’s something oddly humbling about a really hot day. You can have plans, motivation, places to be—and then the temperature hits 40°C and suddenly your only personality trait is finding a fan. But humans aren't the only ones struggling. Animals have to deal with the same rising temperatures, yet they don't all handle heat in anything close to the same way. Some sweat, some pant, some hide in the shade, and some basically rearrange their entire day to avoid the hottest hours. So why didn't evolution just give everyone the same cooling system?

For humans, sweating is a big deal. When sweat evaporates from the skin, it takes heat with it and helps cool us down. The annoying catch is that this works much less efficiently when the air is very humid. So you can be sweating like you've just run a marathon and still feel ridiculously hot.

Animals have their own solutions. Dogs rely heavily on panting, using evaporation from their respiratory tract to lose heat. Other animals may change their behaviour instead—finding shade, reducing activity or becoming active at cooler times of the day. Some species are naturally better adapted to hot environments than others.

Even body size, fur, age and habitat can change the equation. And animals aren't necessarily trying to “cool down” in the same way we are. Sometimes the smartest strategy is simply not getting overheated in the first place.

Humans do this too, of course. We close the curtains, stay indoors, drink something cold and suddenly become extremely interested in whether the air conditioner is actually working.

The problem comes when heat lasts too long. Our bodies have to work harder to get rid of excess heat, placing extra strain on the heart and other organs. High humidity, little airflow and hot nights can make the situation even harder because the body gets fewer opportunities to lose heat.

“A heatwave isn't simply “hot weather.” It's a challenge to an animal's entire way of managing body temperature.”

Every species has its own strategy, shaped by where it lives and how it evolved. Some have built-in cooling tricks that would make us jealous; others rely more on behaviour to escape the heat.

And humans? We got sweating, air conditioning and the ancient survival instinct of saying, “It's too hot, I'm not going outside.”

Rabies is one of those diseases that seems almost unfair. We have vaccines, effective treatment after exposure, and ways to prevent most infections—and yet people still die from it every year. The reason is a strange race against time. Once the rabies virus reaches the central nervous system and symptoms begin, the disease is almost always fatal. Before that point, however, modern medicine can often stop it completely. So how can the same disease be both preventable and so deadly?

Rabies is caused by a virus that is usually transmitted through the saliva of an infected mammal, most commonly through a bite. After entering the body, the virus doesn't immediately cause the dramatic symptoms people associate with rabies. It can spend weeks or even months making its way towards the nervous system.

And this is where the timing becomes incredibly important.

If someone is exposed, post-exposure prophylaxis (PEP) can stop the virus before it establishes infection in the nervous system. Depending on the situation, this involves thorough wound cleaning, rabies vaccine and rabies immunoglobulin or another recommended antibody treatment. When given appropriately before symptoms begin, PEP is highly effective.

The problem is that people may not realise an exposure was serious, may delay seeking medical care, or may not have easy access to the treatment. Rabies is particularly important in parts of Asia and Africa, where dog-mediated transmission remains a major source of human cases.

Once the virus has reached the brain and clinical symptoms appear, our options become extremely limited. That's what makes rabies so unusual: there is a window where prevention works remarkably well, followed by a point where the situation changes dramatically.

Rabies isn't some unbeatable virus. In fact, that's what makes it so frustrating. We know how to prevent it.

The problem is making sure that prevention happens in time. A seemingly minor animal bite can therefore become a race against a virus that moves quietly through the nervous system.

“Sometimes, the most important part of medicine isn't finding a cure—it's getting the right treatment before you need one.”

You know that moment when you finish a big meal and suddenly your brain goes, “You know what would be great right now? A nap.” One minute you're eating, the next you're struggling to keep your eyes open. It's so common that we even have names for it—food coma, post-lunch crash, the works. But why does a perfectly normal biological activity make us feel like we've just worked a twelve-hour shift? And no, it's not simply because all your blood has abandoned your brain to deal with your lunch.

Digestion is actually a pretty busy operation. After you eat, your body releases hormones and other chemical signals to help manage digestion, blood sugar and energy storage. The nutrients entering your bloodstream also affect hormones such as insulin, which helps your cells take up glucose.

What you eat and how much you eat can matter too. A large, energy-heavy meal can make that sleepy feeling more noticeable, particularly if it contains lots of refined carbohydrates or is easy to overeat. Some meals also influence chemicals involved in sleepiness and alertness.

But there's another culprit quietly sitting in the background: your circadian rhythm. Our biological clock naturally produces a dip in alertness in the afternoon. So if you eat lunch right around the time your brain was already considering a tiny shutdown, the combination can feel pretty brutal.

And then there's sleep itself. If you didn't get enough the night before, even a completely ordinary meal can suddenly become the final boss of staying awake.

Getting sleepy after eating doesn't necessarily mean your body is “using all its energy to digest food.” It's more complicated—and honestly, more interesting.

Your meal, hormones, digestion, body clock and how well you slept can all join forces to produce that familiar ‘I just need five minutes' feeling.

So if you've ever blamed lunch for making you sleepy, you weren't completely wrong.

“Lunch just might be getting blamed for a crime your body clock also helped commit.”

Antibiotics are basically the superheroes of modern medicine. Bacterial infection? Take the right drug and boom, problem solved. Except bacteria are not exactly known for being cooperative. Some of them can survive medicines that used to kill them, and those survivors can go on to multiply. This is antibiotic resistance, and it turns something as ordinary as treating an infection into a much bigger problem. The strange part? The microbes aren't sitting around holding a tiny meeting and planning their revenge. It's evolution doing its thing.

Imagine a bacterial population as a very large, very microscopic crowd. Most are vulnerable to a particular antibiotic, but a few may already carry genetic changes that help them survive. The medicine wipes out the susceptible ones, while those few lucky survivors remain.

And then they multiply.

Suddenly, the population that used to be mostly easy to kill contains many more bacteria carrying the survival trait. This is natural selection on a microscopic scale—and honestly, watching evolution happen because of a medicine that was actually designed to stop it is a little ironic.

Resistance can also spread between bacteria when they exchange genetic material. So one microbe doesn't necessarily have to figure everything out from scratch and go through the ‘DIY’ phase.

“Sometimes it can basically get the biological equivalent of forwarding an email.”

The bigger problem is when these medicines are used unnecessarily or incorrectly. Repeated exposure creates more opportunities for those pesky resistant microbes to survive and spread. If enough treatments stop working, infections that were once relatively straightforward can become much harder to manage. It can even make things like major surgery, chemotherapy and organ transplants riskier because effective infection control depends heavily on these drugs.

Antibiotic resistance isn't bacteria becoming smarter or “fighting back.” It's survival and evolution playing out on a scale too small for us to see.

And that's what makes it such a strange problem: we created medicines powerful enough to change medicine itself, but evolution is constantly trying to keep up.

So the next time someone casually says, “It's just an antibiotic,” remember—there's an entire evolutionary arms race happening in the microscopic world.

Here's a weird thing to think about when you're bored out of your mind: you are not alone in your own body. A bit scary- isn't it? Trillions of tiny microorganisms live on you and inside you, especially in your gut. Bacteria, fungi and other microbes are basically sharing your body like a very crowded apartment complex and most of them are actually helping keep the place running. We call this whole community the microbiome. And no, it doesn't mean you're secretly just 30% bacteria and 70% water walking around pretending to be human. But these roommates that aren't visible to you do have a surprisingly big influence on how your body works.

A huge part of the microbiome lives in your gut, where these microbes help break down parts of food that our own enzymes can't fully digest. In the process, they produce useful substances, including something called 'short-chain fatty acids', which can support the cells lining your gut and influence metabolism and immune function.

Your gut microbes also interact with your immune system. They teach lessons about what belongs in the body and what might be a problem, while competing with harmful microbes for space and resources.

“Basically, your gut has its own microscopic neighbourhood watch.”

And it gets even more interesting: scientists are studying the gut-brain connection, because signals from gut microbes can interact with the nervous system and influence things like appetite, stress and mood. This doesn't mean your bacteria are literally deciding whether you're having a good day—but they may be part of a much bigger conversation between your gut and brain.

We usually think of emotions as a very human-y thing. We cry our eyes out when we're sad, hug our friends and family when we miss them, and somehow manage to get emotionally attached to animals who would probably eat our food and then stare at us like we owe them more. But what if animals experience some of these feelings too? A dog waiting by the door, elephants staying beside a dead companion, or chimpanzees comforting each other all raise the same strange question: wait— are animals actually feeling these emotions or what?

The more scientists observe animals, the more complicated the answer becomes.

Take chimpanzees. They have been seen comforting distressed group members through things like touching and staying close to them. And interestingly, not every chimp does it in exactly the same way. Some seem much more likely to comfort others than their companions. Basically, even chimps might have their own versions of “the emotionally available friend.”

Elephants are even more fascinating. They can help injured members of their group, react to distress in other elephants and sometimes spend time around the bodies of elephants that have died. Orcas and other highly social animals have also shown unusual behaviour after losing companions.

And friendship? Animals obviously aren't sitting around exchanging friendship bracelets, but many species form strong, long-term relationships. They choose certain individuals to spend time with, cooperate with them and sometimes even seem to prefer particular companions.

Grief is the tricky part. We can observe what an animal does, but we can't exactly sit an elephant down and ask, “So… how are you feeling about this?” Scientists therefore talk about grief-like behaviour rather than claiming they know exactly what is happening inside the animal's mind.

Maybe animals don't experience emotions in exactly the same way we do. But the more we study them, the harder it becomes to say that their social lives are simply instinct and nothing more.

And honestly, maybe friendship doesn't always need words, matching bracelets or a daily 2-hour chat.

“Sometimes it might just mean choosing to stay beside someone.”

We all know we're supposed to exercise. Move more, sit less, get your steps in—the usual advice. But have you ever actually stopped to think about what happens in your body when you decide to stop being a couch potato and exercise? Because the whole thing is kind of crazy. The second you start running, your heart suddenly goes into overdrive, you're breathing like you've just escaped a hungry dog, and your legs are questioning your life choices. Meanwhile, inside your body, a whole team of systems is working together. And if you keep exercising regularly, they actually start getting better at their jobs.

Let's start with the heart and lungs. The moment you start moving, your muscles need more oxygen and energy. So your heart pumps faster and your breathing picks up to get more oxygen into your blood and move it where it's needed. Do this regularly, and your heart gets more efficient at pumping blood, while your muscles get better at using oxygen.

Your muscles also adapt to being challenged. They become stronger and better at handling the same workload. Even your bones respond to regular weight-bearing movement by getting signals that help maintain their strength. Which is funny when you think about it—your bones are technically getting a workout too.

And then there's the brain, the big bad wolf. Exercise increases blood flow to the brain and affects chemicals involved in mood, stress and attention. So that post-walk feeling of “okay, I can deal with my life again” isn't completely in your head. Well… technically it is, because your brain is involved.

Exercise also helps your metabolism work more efficiently, including improving how your cells respond to insulin and use energy.

The coolest part is that exercise isn't just about getting stronger or burning calories. Your body is constantly noticing what you ask it to do and adjusting accordingly.

Your heart, lungs, muscles, bones, brain and metabolism all gradually adapt.

“So yes, exercising can be miserable and brutal sometimes—but your body is quietly turning that struggle into an upgrade.”

We spend roughly a third of our lives sleeping, which is honestly a little crazy when you think about it. That’s years spent lying completely still, eyes closed, apparently doing absolutely nothing. Except… our bodies are actually working overtime. Sleep is when the brain switches between different stages, sorts through information, regulates hormones and helps the body recover. So sleep isn't the brain pressing an “off” button. It’s more like the night shift has started—and the brain has a pretty long to-do list.

Before we even fall asleep, our circadian rhythm, basically the body's internal 24-hour clock, starts preparing us. As it gets dark, the brain increases melatonin which helps signal that it’s time to sleep. Meanwhile, a chemical called adenosine gradually builds up while we’re awake, creating something called sleep pressure. So that 2 a.m. “I could literally sleep while standing up at this point” feeling? There’s biology behind it.

Once asleep, the brain moves through non-REM and REM sleep in cycles that repeat several times. Deep non-REM sleep is especially important for physical recovery, while REM sleep is associated with vivid dreaming, learning and processing information. Interestingly, we tend to get more deep sleep earlier in the night and more REM sleep later.

Sleep also helps strengthen and organise memories. So that chapter you desperately crammed at 11 p.m.? Your brain may actually work on organising it while you sleep.

Meanwhile, your heart rate and breathing generally slow down, body temperature drops slightly, muscles relax, and hormones involved in growth, appetite, metabolism and stress are regulated. Even your immune system gets a night shift.

And this is where “I’ll sleep later” becomes questionable. Too little sleep can affect attention, reaction time, mood, learning and memory. Repeatedly getting too little sleep can also interfere with immunity and is associated with longer-term health problems.

Sleep isn't wasted time, even though it can feel like you're accomplishing absolutely nothing. Your brain is organising memories, your body is recovering, and several systems are quietly resetting. So the next time you sacrifice sleep for one more episode or another late-night study session, remember: your brain has a night shift too.

“And apparently, it doesn't believe in unpaid overtime.”

You know that feeling you get when you have an exam tomorrow, 47 tabs open, three deadlines approaching, and suddenly your heart decides it wants to run a marathon while your stomach makes weird noises? Yeah, that's stress. And while we usually describe it as something that is “in our head”, the rest of the body clearly didn’t get the memo. Your heart speeds up, your breathing changes, your stomach starts acting suspicious, and your brain goes into full alert mode. So, what exactly is going on? Or more precisely, what exactly happens inside us when stress takes over?

It starts when the brain senses a threat or challenge. It could be something genuinely dangerous, like seeing a tiger on the loose, or something way less dramatic—like your teacher saying, “Put your pens down.” Your brain sends out an alarm, activating the body's fight-or-flight response. The adrenal glands release hormones such as adrenaline, which quickly gets the body ready to react. Your heart beats faster, breathing speeds up, blood flow is directed towards your muscles, and more glucose becomes available for energy. Basically, your body temporarily prioritises survival over everything else.

Then comes cortisol, another stress hormone that helps keep the body on high alert for longer. This is useful when you actually need to deal with a threat. The problem begins when the alarm doesn't seem to switch off. If stress keeps happening again and again, the body spends too much time in this high-alert state, which can interfere with things like sleep, digestion, immunity and concentration.

That being said, stress isn't automatically the villain. A little can sharpen your focus and even give you that extra push when you need it. The real problem is when your body's emergency alarm starts acting like it pays rent and refuses to leave. Your body is built to handle stress—but it also needs a chance to switch off, recover, and breathe. After all, like they all say, excess of anything is bad.

Having a fever feels like being stuck in a daily soap—overly dramatic, unpredictable, and seemingly never-ending. One moment your body is shivering under a foot-thick blanket and the next it starts sweating like you've been running a marathon. Everyone keeps repeating, "You are burning up!" So what exactly is happening? Your body is not simply overheating like an old, used-up machine; it is doing a planned defense move, something like a samurai. It has found a problem and thus, decided it is time to change the default settings.

When the immune system finds an infection, it does not simply wait. It releases chemical signals that send an alert to the brain. The alert reaches the hypothalamus, which can be thought of as our bodies' thermostat.

Normally, the body keeps temperature close to 37 °C. When an infection occurs, our bodies raise that setting temporarily.

That explains something: the shivering.

If the brain suddenly sets 39 °C as the new target temperature, the body can feel cold at 37 °C. The body then shivers, reduces heat loss by constricting blood vessels and makes us want to reach for seventeen blankets.

When body temperature reaches the target, the chills usually stop. Then, when the brain lowers the thermostat, the body needs to get rid of the extra heat. Sweating, skin flushing and the need to throw off those seventeen blankets follow.

So a fever is not the body randomly going haywire. It is the immune system, the brain and the body working together on a coordinated project—except nobody asked the body to participate. It can feel awful. The rise in temperature is just part of a larger response to whatever is making the body sick.

“The body is not just getting hotter, it is changing the rules of the game.”