We’ve got three fascinating scientific developments to catch you up on!

Our team picked three great scientific breakthroughs that could have an impact on health, so you can stay in the loop, Eureker!

The stories we’re covering are: a diet that may “reprogram” one of the deadliest childhood cancers, a non-hormonal reversible male contraceptive getting closer to reality, and a fascinating finding about gaining weight when you’re young that you’re probably going to want to share with everyone.

Now, let’s dive in!

1) A reversible, non-hormonal male contraceptive!

Scientist, did you know that the main established contraceptive options available to men are still condoms and vasectomy? This hasn’t changed much in decades.

Vasectomy is intended to be permanent and long-lasting. Although it can technically be reversed surgically, reversal isn’t guaranteed, so most people consider it a permanent form of contraception.

And what about hormonal methods for men? They’ve been tested in multiple studies over the years, but development has repeatedly run into problems because of side effects, including mood changes and depression.

But a study published in April 2026 in the Proceedings of the National Academy of Sciences by researchers at Cornell University may represent an important step toward changing this landscape.

The researchers investigated a compound called JQ1 (chemical structure shown above) as a way to temporarily disrupt meiosis, a specialized form of cell division involved in sperm production, without causing lasting damage.

The results were promising: researchers administered JQ1 to male mice for three weeks. The animals stopped producing sperm. After treatment was discontinued, normal sperm production returned within six weeks. The researchers then bred the mice and confirmed that they were fertile, and their offspring were completely healthy.

JQ1 itself will not be the final product: its neurological side effects rule it out for human use. It served as a proof-of-mechanism tool, rather than a drug candidate. But the team has already identified three promising new genetic targets without these effects and plans to launch a company within the next two years.

If it eventually reaches the market, a male contraceptive could potentially be administered as an injection every three months, or possibly as a patch!

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For now, though, this is still mouse research, and there are important biological differences between mice and humans. The road from an interesting result in animals to a real-world contraceptive is a long one.

2) Does gaining weight before age 30 increase the risk of premature death by 70%?

What’s worse: gaining weight in your 20s or in your 50s?

Honestly, neither sounds like a particularly great option, does it?

A study published in April 2026 in The Lancet, led by researchers at Lund University in Sweden, investigated how changes in body weight over time relate to mortality.

The study followed more than 600,000 people. Participants were included only if their weight had been measured at least three times. For example, during pregnancy, military recruitment, or participation in research studies.

People who developed obesity between the ages of 17 and 29 had approximately a 70% higher risk of premature death compared with those who did not develop obesity before age 60.

The leading cause of death associated with early-onset obesity was type 2 diabetes, followed by hypertension and liver cancer in men and uterine cancer in women.

The study was observational, so it does not prove causation, and it was conducted predominantly in a Swedish population, which may limit how broadly the findings apply to other populations and contexts.

3) Could an unusual combination of a drug and a controlled diet reprogram one of the deadliest childhood cancers?

Scientist, have you heard of neuroblastoma?

Treating high-risk neuroblastoma remains one of the major challenges in pediatric oncology. That’s why a study involving the patients’ diet attracted so much attention from the scientific community.

Before we go any further: no, we’re not talking about a diet that cures cancer. We’re talking about a pharmacological strategy developed and tested in animal models, in which a carefully controlled dietary restriction is part of a medical intervention. That is very different from anything someone should try at home.

The researchers’ clever move was to shut down those alternative routes too.

They combined DFMO with a proline- and arginine-free diet: two amino acids that can be obtained through the diet and that the tumor can use as building blocks to produce polyamines.

With this double intervention, the tumors were deprived of an essential precursor while eflornithine blocked the remaining escape route.

With polyamines depleted, the tumor’s protein-making machinery began producing fewer proteins associated with cell division and more proteins associated with neuronal growth and maturation.

It was almost as if, without the right fuel, the tumor had “forgotten” that it was cancer and started following its original developmental program again.

The study was conducted entirely in genetically modified mice, and the distance between this result and a clinical trial in children is still enormous!!

Maintaining a proline- and arginine-free diet for long periods also presents serious nutritional challenges in pediatric patients, which would need to be addressed extremely carefully.

Science hasn’t been sitting still, and neither have we!

When we founded Eureka, the idea was simple: what if science could be explained with the same enthusiasm we use when talking about football?

Every piece we publish is an attempt to prove that this is possible. You don’t need a PhD to understand what research says about your body, your health, and your life.

But for that message to reach more people, we need you.

Share this post. Send it to the family group chat. To the friend who thinks science is boring. To the person who keeps falling for health misinformation. Every share is a vote for the idea that knowledge matters.

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And tell us: what did you think of this edition? Was there a story that surprised you? Something that wasn’t clear? Something you’d like us to explore further?

Leave a comment below… we read everything!!

Eureka is built together with you. 🧬❤️

Have an excellent weekend, Scientist. And keep an eye out for more science!

Let’s start our morning with coffee, history… and one of the biggest tragedies in chemistry and medicine.

That is exactly the story of thalidomide.

Back in the late 1950s, thalidomide was introduced as a “safe” sedative, including for pregnant women experiencing morning sickness. It worked. The problem was that nobody had paid attention to something fundamental about it.

It wasn’t really just one molecule. In practice, there were two “versions” of it, what chemistry calls enantiomers. And here comes a key concept you may have seen back in high school (we promise chemistry can be interesting!).

The difference between the molecules is basically a seven one-error game. The molecules look identical, but they aren’t. They are tridimensional, and this tiny change in their orientation in space can make all the difference to their biological effects.

In the case of thalidomide, one enantiomer had therapeutic effects. The other was teratogenic, meaning it could interfere with embryonic development and cause congenital malformations.

And here’s where chemistry can be particularly cruel: even if you administered only the “good” version, one form could convert into the other inside the human body in a process known as interconversion.

Observe that Y and W switch positions between the two structures. Even though the same atoms are attached to the central carbon, this inversion creates two molecules that are mirror images of each other but cannot be perfectly superimposed. That’s exactly what we call enantiomers.

And that’s how, unknowingly, doctors prescribed a drug that resulted in thousands of cases of congenital malformations, particularly affecting the limbs.

It is estimated that more than 10,000 babies were affected worldwide. Images can be found on the Wikipedia page for thalidomide, but they may be disturbing.

Thalidomide became a symbol of a massive medical error.

But the story doesn’t end there.

Decades later, scientists began to investigate more carefully how it worked. They discovered that thalidomide has very specific effects on the immune system and blood-vessel formation. In other words, it can reduce inflammation and also interfere with the growth of new blood vessels that supply tissues, including tumors.

That’s why thalidomide is still used today, but only in very specific and tightly controlled circumstances.

Thalidomide also gave rise to a new generation of drugs, including lenalidomide and pomalidomide, which are used to treat cancers such as multiple myeloma.

These drugs are called immunomodulatory agents (IMiDs) and work in a fascinating way: they bind to a protein called cereblon, which helps “tag” other proteins inside the cell for destruction. By interfering with this process, they can eliminate proteins that are important for tumor-cell growth while also modulating the immune system. It’s an incredibly sophisticated mechanism!!! but that story is for another day…

These medications are more “refined.” They retain the desired therapeutic effects but were developed to be safer and more predictable.

But it’s important not to romanticize this story. The use of thalidomide today is surrounded by extremely strict regulations: prescription controls, continuous medical monitoring, and, above all, an absolute prohibition during pregnancy.

This is a story about a mistake, but also about learning from that mistake.

Thalidomide changed the way medications are tested and approved (you can read more here!). After this disaster, regulatory requirements became much stricter, particularly regarding potential effects on embryonic development. In other words, part of the safety we have in medicine today was built in response to this disaster.

So, what did we learn?

• First, those tiny differences in chemistry can have enormous consequences for biological effects.

• Second, that no medication is “simply good” or “simply bad.” Everything depends on the context, the dose, and who is taking it.

• And third, that when you see a substance being repurposed or “rediscovered,” it isn’t a miracle or something suspicious. Drug repurposing is a common concept in pharmacology, and we also discussed it in our post about ivermectin .

And if you enjoyed starting your morning with science, share this story with someone who would find it interesting too.

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Here at Eureka, we dream of making science as popular as soccer. Every day, we try to bring you stories that genuinely add something to your life! Subscribe and share to help us keep that dream alive!

Today, we’re going to look at three studies published in some of the world’s leading medical journals. Together, they raise an urgent warning: a silent epidemic of cancer is growing among adults under 50.

But before we start, have you subscribed to Eureka yet? No???? Then go subscribe already!

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Alright. LET’S GO!

You’ve probably heard stories that seem “out of the ordinary”: a 38-year-old friend diagnosed with colorectal cancer, a 32-year-old cousin with breast cancer, a 44-year-old coworker dealing with pancreatic cancer. What once sounded like an extremely rare exception is gradually becoming part of everyday life.

And it’s not just your imagination. The science confirms it: we are seeing a real increase in cancer among younger people.

Articles published in Nature Reviews Clinical Oncology, The Lancet Oncology, and BMJ Oncology paint an alarming picture — but also one full of clues about what may be happening to our health.

📈 The numbers that should be making headlines

Let’s start with the most striking data, which comes from the study published in BMJ Oncology. Researchers analyzed the Global Burden of Disease (GBD 2019) database, covering 29 types of cancer across 204 countries over three decades.

The result:

• Between 1990 and 2019, the number of new cancer cases diagnosed in people under 50 increased by 79.1% globally in absolute terms.

• The number of deaths from these cancers increased by 27.7% over the same period.

• In 2019 alone, there were more than 3.26 million new diagnoses and 1.06 million deaths among younger people.

And the near future doesn’t look particularly promising: if current trends continue, the researchers project that the number of new cancer cases in younger people will increase by another 31% by 2030, while cancer-related deaths are expected to rise by 21%.

If these numbers were from any other disease, they’d be making headlines everywhere.

🦠 So, which cancers are increasing the most?

The Nature Reviews Clinical Oncology study identified 14 types of cancer with notable increases among younger adults since the 1990s. They include:

• Breast cancer

• Colorectal cancer

• Endometrial cancer

• Pancreatic cancer

• Liver cancer

• Kidney cancer

• Prostate cancer and thyroid cancer

Breast cancer continues to have the greatest global burden, with more cases and more deaths among younger people. But prostate and nasopharyngeal cancers showed the steepest increases since 1990.

There is one positive exception in this otherwise gloomy picture: early-onset liver cancer was the only cancer that showed a consistent decline in incidence. One plausible explanation is the impact of hepatitis B vaccination programs, since vaccination reduces the risk of liver cancer later in life 💉.

🧬 Why is this happening? The “early-life exposome” theory

This is where we get to the heart of the story:

Researchers in Nature Reviews introduce a concept called the exposome: the totality of everything we are exposed to throughout our lives: our diet, chemicals, medications, microorganisms, stress, pollution, and more.

The central hypothesis is powerful: what happens early in life, from conception through adolescence, may influence cancer risk decades later.

Think about it: someone born in the 1990s grew up in a radically different world from someone born in the 1950s. The environmental and lifestyle changes that intensified throughout the second half of the 20th century may be coming back to collect the bill.

And earlier than we expected.

So, what are these changes?

The studies point to a combination of interconnected factors:

🍔 Ultra-processed foods and the Westernization of our diets

Diets high in ultra-processed foods, saturated fats, red meat and sugar, and low in fiber and vegetables. Excessive consumption of sugary drinks also enters the equation. It’s probably not a coincidence that many of the cancers showing the greatest increases affect the digestive system.

Thought you were going to pick the salad? Nice try, sucker!

⚖️ Obesity and a metabolism out of control

The increase in childhood and adult obesity, type 2 diabetes, and physical inactivity creates a hormonal and inflammatory environment that can promote tumor growth.

🦠 The microbiome in crisis

This may be one of the most underestimated (and least studied) factors. Changes in the gut microbiota (dysbiosis), associated with poor diet, physical inactivity, and excessive antibiotic use, have been linked to 8 of the 14 cancer types identified, particularly cancers of the digestive system.

Changes in the microbiome are one of the most relevant hypotheses, especially because many of the rising early-onset cancers involve the digestive system. But longitudinal studies are still needed to separate cause, consequence, and correlation.

🌙 Reproductive and lifestyle factors

Earlier menarche (getting your first period at a younger age), less breastfeeding, having a first child at an older age, altered sleep patterns, alcohol consumption, and smoking (including exposure to tobacco smoke in the womb) complete the picture.

📊 The special case of colorectal cancer: a warning for the whole world

The study published in The Lancet Oncology focused specifically on colorectal cancer (CRC), analyzing data from 50 countries and comparing two age groups: adults aged 25–49 and adults aged 50–74.

The finding is revealing and counterintuitive: while CRC rates are falling or stabilizing among older adults, thanks in part to screening programs such as colonoscopy, they are consistently increasing among younger people.

In other words: we’ve managed to control the disease in people who are being screened, but it continues to quietly emerge in people who aren’t on the screening radar.

Other important details:

• The increase is particularly strong in high-HDI countries, including the UK, Australia, and parts of Europe: the same countries that have experienced widespread adoption of Western lifestyle patterns.

• In developing countries, rates are increasing in both age groups, as these countries adopt Western habits without necessarily having the same screening infrastructure.

• The increase is more pronounced in the rectum and left side of the colon, details that may help researchers better understand the mechanisms involved.

• Risk is increasing with each successive generation born since the 1950s, something epidemiologists call a “birth-cohort effect.” Each more recent generation appears to be starting life with an accumulated disadvantage.

Because of this, countries such as the US and Australia have already lowered the recommended starting age for CRC screening from 50 to 45. Others may follow.

⚠️ The problem with “you’re too young to have cancer”

One of the most critical points raised by the researchers is delayed diagnosis among younger adults. Doctors and patients are less likely to associate classic cancer symptoms, such as rectal bleeding, changes in bowel habits, persistent fatigue, and abdominal pain, with cancer when the person is in their 30s or 40s.

The result? Later diagnoses, when treatment is more difficult and outcomes are worse.

🌍 Where is the situation most serious?

The GBD 2019 data show that the highest incidence rates among younger people in 2019 were recorded in North America, Australia, and Western Europe: regions strongly associated with sedentary lifestyles and high consumption of ultra-processed foods.

But the highest mortality rates among younger people were found in Oceania, Eastern Europe, and Central Asia: regions where access to early diagnosis and high-quality treatment is more limited.

This shows that the epidemic is global, but its most devastating consequences fall disproportionately on people with fewer resources.

🔬 What science still doesn’t know

It’s important to be honest: there is still a lot we don’t know.

Researchers recognize that the long latency period between exposure (potentially during childhood) and diagnosis decades later makes it difficult to isolate the exact effect of each individual risk factor.

In addition, early-onset cancers appear to have distinct molecular characteristics compared with cancers that develop at older ages. This suggests that they may respond differently to existing treatments. Longitudinal research, with long-term follow-up using biobanks and electronic health records, is urgently needed.

💡 So, what can we actually do with all of this?

The studies are clear in their recommendations, and they operate on two levels:

For society and governments:

• Expand screening programs to include younger age groups.

• Implement public policies that promote healthy eating and reduce alcohol and tobacco use from childhood onward.

• Invest in longitudinal research to better understand the causes.

For you, individually:

• Take care of your gut: eat a balanced diet with plenty of fruits, vegetables, whole grains, and fiber, and fewer ultra-processed foods.

• Avoid overweight and obesity.

• Move your body: physical inactivity is a real, modifiable risk factor, while exercise reduces cancer risk.

• Reduce alcohol consumption and avoid cigarettes, e-cigarettes, and hookahs, including secondhand exposure.

• Pay attention to your body and don’t ignore persistent symptoms.

• Use sunscreen.

• Get vaccinated against HPV.

• If you have gastric symptoms, consider testing for H. pylori.

• Talk to your doctor about cancer screening, especially if you have a family history of any type of cancer.

  ---

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Today we’re sharing a few tips that might help you stay out of the emergency department.

But first, if you’re new here, subscribe to Eureka! Free science, delivered to your inbox every day. What more could you ask for?

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Now let’s get started!

If you ask an emergency physician what scares them the most, the answer is rarely an exotic virus or a rare medical condition. It’s not fear of the unknown… it’s exactly the opposite! It’s familiarity.

It’s the feeling of having seen the same story countless times before. Knowing exactly how it started. These are accidents that happen in seconds, in places we consider safe, and that could often have been prevented with a simple change in behavior.

TIME Magazine recently spoke with emergency physicians about the common situations that bring people to the emergency department—many of them hidden in our own homes and daily routines. Here are the key lessons every Eureker should know.

1. The symptom that was ignored for months: persistent abdominal pain or a cough that won’t go away

Symptoms that linger for days, weeks, or even months are often dismissed. Dr. Evelyn Huang, from Orlando, says she regularly sees patients with advanced diseases after they ignored subtle warning signs such as a persistent cough or ongoing abdominal pain.

The rule is simple: if something has changed from your usual state of health and doesn’t improve, don’t wait until it becomes an emergency to have it evaluated.

2. Childhood drowning: a few seconds of distraction can be fatal

Drowning is one of the leading causes of accidental death among children aged 1 to 4 in the United States. Dr. Cheyenne Falat says parents often tell the same story: “I thought someone else was watching.”

Early swimming lessons, which can teach infants how to roll onto their backs and float, may help reduce the risk, although they never replace constant adult supervision. Pool fences with self-latching gates and clearly assigning one adult to watch the child are equally important.

3. Laundry detergent pods are more dangerous than most people realize

Dr. Jeff Yoo is particularly concerned about detergent pods. Because they are highly alkaline and contain concentrated irritants (often with a pH above 10), they can cause severe chemical burns to the mouth, eyes (especially the cornea) and other mucous membranes.

If a pod bursts while being handled, it can spray detergent directly into the eyes. Without prompt treatment, this can even result in permanent vision loss. Swallowing these products can also be extremely dangerous, especially for children.

Eureka Concept 🧠

Why is the cornea so vulnerable?

The cornea is the transparent front surface of the eye. It protects the structures inside the eye while also performing most of the light refraction needed for clear vision. Because it contains no blood vessels—allowing it to remain transparent—it relies on tears and the aqueous humor for nutrients. Its high protein and collagen content also makes it particularly vulnerable to alkaline chemical burns, which can permanently damage its clarity and impair vision.

4. “It was just a simple fall from a ladder...”

A fall from just one story can be enough to cause fractures, deep lacerations, or traumatic brain injuries. Dr. Jordan Wagner, an emergency physician and one of the creators of ER, says ladder falls are incredibly common. The same applies to equipment such as lawn mowers and other power tools. Many injuries occur when people try to unclog or repair machinery without turning it off first.

5. Heat and cold can both be deceptive

Extreme weather isn’t the only danger. Cold-related injuries and hypothermia don’t occur only during harsh winters. They can also develop in spring or fall, when temperatures suddenly drop after a warm day and clothing remains damp with sweat.

Heat can be just as dangerous. “Heat-related illness exists on a spectrum—from mild dehydration to heat exhaustion and, in the most severe cases, heat stroke, which can be fatal,” says Dr. Falat.

The biggest warning signs are neurological symptoms such as confusion or disorientation. At that point, it’s a medical emergency.

6. Lightning: don’t take a photo—go inside!

Dr. Falat also frequently treats lightning-related injuries. Lightning doesn’t only strike people directly. The electrical current can travel through the ground, trees, and metal objects. If you notice buzzing in the air, smell something metallic, or feel your hair standing on end, don’t pull out your phone to take pictures. Get indoors immediately.

7. GHB: the line between euphoria and coma

Dr. Jeff Yoo also warns about gamma-hydroxybutyrate (GHB), commonly known as “liquid ecstasy.” Colorless, odorless, and tasteless, GHB can be slipped into a drink without being noticed. The difference between a dose that causes relaxation and one that causes an overdose is alarmingly small. Patients often arrive unconscious after a night out, alternating between coma, severe agitation, and respiratory failure. Some require emergency intubation.

Never accept an open drink from someone you don’t know.

Quick Survival Checklist 🏥

Here are the key take-home messages:

• Listen to your body. Persistent symptoms (such as a cough, abdominal pain, or ongoing fatigue) deserve medical attention if they don’t improve.

• Take water safety seriously. Drowning is silent. Never assume someone else is watching the child. Use pool fencing, assign one adult to supervise, and consider early swimming lessons.

• Handle cleaning products with care. Concentrated detergent pods can cause severe chemical burns. Keep them away from children, avoid squeezing or separating stuck pods, and never mix household cleaning products.

• Respect ladders and power tools. Always switch equipment off before attempting repairs or clearing blockages. Even relatively short falls can cause life-threatening injuries.

• Protect yourself from extreme temperatures. Wet clothing in cool weather can contribute to hypothermia, while confusion after heat exposure is a warning sign of heat stroke, which requires urgent medical care.

• Take thunderstorms seriously. If you notice signs that lightning is nearby, seek shelter immediately instead of stopping to record the storm.

• Stay alert when you’re out. GHB is invisible, odorless, and can cause life-threatening overdose. Never accept an open drink from a stranger, and always keep an eye on your own drink.

Which of these tips surprised you the most, or do you think is most commonly overlooked?

If you found this helpful, share it with friends to help spread evidence-based health information.

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Ready to start the day with a cup of coffee and a dose of science? ☕🧫🧬

Better yet, why not start every morning with evidence-based science?

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Now, let’s dive in!

Over the past few years, ivermectin has worn many hats.

It is a Nobel Prize-winning antiparasitic medication (we’ll get to that story in a moment), became the center of major controversy during the COVID-19 pandemic, and has now reappeared in a new wave of social media claims.

Can ivermectin treat cancer?

The short answer is:

But the story is worth exploring.

Ivermectin is an established antiparasitic medication used to treat infections caused by worms and certain parasites.

Chemical structure of ivermectin.

Its discovery was so important that it earned the 2015 Nobel Prize in Physiology or Medicine, thanks to its revolutionary impact on neglected tropical diseases such as onchocerciasis (river blindness), a disease caused by the parasite Onchocerca volvulus.

The story began in the 1970s, when Japanese microbiologist Satoshi Ōmura collected soil samples in search of bacteria capable of producing useful medicines. One of those samples yielded a bacterium called Streptomyces avermitilis, which produced compounds with remarkable antiparasitic activity. Those compounds were later refined by William Campbell in the United States, ultimately leading to the development of ivermectin.

The 2015 Nobel Prize in Physiology or Medicine was awarded jointly to William C. Campbell and Satoshi Ōmura for discoveries leading to new therapies against parasitic diseases, and to Tu Youyou for the discovery of artemisinin for malaria. (Image source: NobelPrize.org.)

Since then, ivermectin has helped prevent blindness in millions of people worldwide. In other words, this is a highly important and well-established medication.

But that doesn’t mean it works for everything.

Where Did the Cancer Claims Come From?

Over the past few years, laboratory studies have suggested that ivermectin can affect certain cancer cells.

In cell cultures, and often at very high, non-physiological concentrations, ivermectin appears to interfere with processes involved in tumor growth, including cell proliferation and survival.

Let’s repeat that:

Not in patients.

These laboratory findings sparked interest in something known as drug repurposing: the idea of testing an existing medication for an entirely different disease.

Unfortunately, this is also where misconceptions begin.

Many compounds show exciting results in isolated cells. Some even perform well in animal studies. Yet most of them never become successful treatments for humans. Sometimes they simply don’t work. Other times, the dose required would be far too toxic for people.

Although laboratory studies have produced interesting findings, clinical studies in humans remain extremely limited. Some ongoing trials are evaluating ivermectin alongside immunotherapy for certain cancers, but no convincing clinical benefit has been demonstrated so far.

At this stage, ivermectin remains a scientific hypothesis, not a cancer treatment.

Why Misinformation Matters

A review published in Cancer Cytopathology highlights how misinformation surrounding cancer treatments can have serious real-world consequences. The authors discuss evidence showing that patients who relied only on unproven alternative therapies experienced significantly higher mortality than those who received evidence-based cancer treatment.

Whenever a potential treatment becomes popular online, some people begin using it before the science has finished answering the important questions. One common narrative circulating online claims that cancer is caused by parasites, and therefore antiparasitic drugs such as ivermectin could “treat the underlying cause.”

There is no scientific evidence supporting this claim.

Public figures have occasionally amplified these ideas. For example, actor Mel Gibson publicly mentioned acquaintances who reportedly improved after taking ivermectin.

However, anecdotes are not scientific evidence.

An Important Lesson

One reason these claims spread so easily is that ivermectin is already a familiar medication. Many people assume that if a drug is approved for one condition, it must also be safe, or even effective, for many others.

That isn’t how medicine works.

The concentrations needed to produce anticancer effects in laboratory experiments are often much higher than the doses considered safe for humans, raising serious concerns about toxicity.

There’s another important point.

Cancer is not a single disease.

It is a collection of hundreds of biologically distinct diseases. A result observed in one cancer cell line does not mean the same drug will benefit patients with different cancers, or even the same cancer, in clinical practice.

What Can We Take Away? ☕

We’re not saying it’s impossible that ivermectin could eventually play a role in cancer treatment.

We’re saying that the evidence simply isn’t there yet.

And when it comes to cancer, acting before the evidence is available can have serious consequences.

The practical message is straightforward:

If you or someone close to you is undergoing cancer treatment, prioritize therapies supported by high-quality clinical evidence and discuss any alternative treatments with your healthcare team.

Perhaps the most important lesson is this:

That’s not a failure of science. That’s exactly how science works: carefully testing ideas until only those that truly help patients remain.

Thank you for reading!

If you found this article helpful, share it with someone who values evidence-based medicine and help combat scientific misinformation.

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If you’ve been following Eureka!EN, you’ve probably read our recent article about the Tuskegee Study, one of the most unethical episodes in the history of clinical research. (And if you haven’t, don’t miss the chance to subscribe to this amazing newsletter!!)

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To complement that article, we’d like to present our Movie of the Month for August: a film based on that true story that helps us understand it through a deeply human perspective.

It’s one of those films that every scientist, healthcare professional, and science enthusiast should watch at least once in their lifetime.

So...

Our Movie of the Month for August is…..

Miss Evers’ Boys.

Rather than following politicians or researchers, the story is told primarily through the eyes of Nurse Eunice Evers, a fictional character inspired by the nurses who cared for the men participating in the study. Through her perspective, we witness an incredibly difficult ethical dilemma:

The true story that changed clinical research

In 1932, the United States Public Health Service recruited hundreds of Black men in Alabama for what they believed was a free healthcare programme. In reality, many of them had syphilis and were never informed of their diagnosis.

Even after penicillin became an effective treatment in the 1940s, researchers deliberately prevented these men from receiving it so they could continue observing the natural progression of the disease.

The study lasted FOUR DECADES!!!

When it was finally exposed in 1972, it sparked worldwide outrage and forever changed the way research involving human participants is conducted.

Why is this film still so relevant?

Miss Evers’ Boys is much more than a historical drama.

It explores issues that remain highly relevant today:

• informed consent;

• racial inequality in healthcare;

• conflicts between science and ethics;

• the responsibility of healthcare professionals;

• and the need to protect people who participate in scientific research.

Many of today’s research ethics regulations were shaped directly by the lessons learned from Tuskegee.

Our favourite part

One of the film’s greatest strengths is that it avoids portraying its characters as simply “good” or “evil.” Instead, it shows how ordinary people can become part of profoundly unethical systems when they stop questioning decisions and authority.

Perhaps that is its most important message:

Science is not defined only by great discoveries. It is also defined by the ethical choices that scientists and healthcare professionals make every single day.

Our recommendation

At Eureka!EN, we believe that understanding the mistakes of science is just as important as celebrating its greatest achievements. Studying cases like Tuskegee does not diminish trust in science.

Quite the opposite.

⭐ Watch it!

And if you haven’t already, be sure to read our article on the Tuskegee Study.

Because real science always begins with respect for human dignity.

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Unfortunately, this is a difficult topic, but an important one to discuss: Science, in partnership with Retraction Watch, published an investigative report about a six-year-old girl in China who died after taking part in an experimental gene-editing trial in the brain. In addition, another death has also been linked to an experimental gene-editing trial.

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First of all: we are deeply saddened by the deaths of both girls, and our thoughts are with their families.

Let’s understand what happened:

What was the treatment?

In the first case, the girl (referred to as “Mei” in the report to protect her privacy) had a rare genetic mutation in the CHD3 gene, which causes Snijders Blok-Campeau syndrome: developmental delay, autism-related characteristics, and mild to moderate intellectual impairment, depending on the case.

After years of searching for answers, her parents contacted Zilong Qiu, a neuroscientist at Xinhua Hospital in Shanghai, who had been developing “base-editing” therapies (a more precise version of CRISPR) for rare diseases.

The proposal: correct the genetic “letter” that had been changed (a T that should have been a C) directly inside the girl’s neurons.

She would become the first person in the world to receive a gene-editing therapy directly in the brain.

Source: Science, 2026.

What went wrong

According to the investigation, the treatment went ahead despite several warning signs, including:

• A safety study in monkeys (completed just one month before the procedure) showed that all four treated animals developed moderate to severe liver damage, and one also developed kidney damage.

• This toxicology report was never reviewed by the hospital’s ethics committee before the study involving the girl was approved.

• Experts interviewed by Science raised concerns about the imaging used to convince the family and the ethics committee that the viral vector was reaching the neurons correctly, without adequate control samples.

Seven days after receiving the infusion (trillions of viruses carrying the genetic-editor instructions, delivered directly into the cerebrospinal fluid) the girl died from a severe immune reaction: thrombotic microangiopathy, a condition involving microscopic blood clots that can be fatal.

Eureka Concept 🧠

Why is editing the brain so much harder than editing the liver?

One of the most famous examples of base editing so far is that of baby “KJ” Muldoon in the United States, who was treated for a metabolic disease. In that case, the gene editor was delivered to the liver through the bloodstream inside tiny lipid particles.

The brain is a different story: it is protected by the blood-brain barrier, which prevents most molecules (including viruses) from moving from the bloodstream into brain tissue.

That is why the Chinese team had to inject the viruses directly into the cerebrospinal fluid, using doses hundreds of trillions of times higher than those used in a typical vaccine, because only a small fraction of the viruses actually enters the target cells.

There was another technical problem: the “base editor” is too large to fit inside a single virus, so it had to be split into two parts, carried by two different viruses. Both viruses needed to reach and act inside the same cells at the same time, substantially increasing the complexity (and the risk) of the procedure.

What happened afterward

According to the report, the institutional response to the case was very different from what happened in other tragic episodes in the history of gene therapy, such as the death of Jesse Gelsinger in the United States in 1999, which led to years of scrutiny of the field.

In Mei’s case:

• The hospital paid a fine of around US$3,600 for failing to properly register the study and did not publicly sanction the researcher responsible.

• A paper published months later in Nature, describing the preclinical work behind the treatment, removed references to the family and their funding and did not mention the liver and kidney problems found in the monkey study.

• The university told the family that the paper “had no connection” to the experiments they had funded.

It is worth noting that, under China’s regulatory system, studies like this one (non-commercial research conducted by investigators within hospitals) go through a considerably less stringent approval pathway than a commercially sponsored study would.

Several experts in genetics, virology, and bioethics interviewed for the report are calling for a complete review of the published data and greater transparency regarding the study’s funding. Some argue that this alone would justify retracting the paper.

Update: this was not an isolated case

After Science’s investigation was published, another Chinese gene-editing company, HuidaGene Therapeutics, confirmed the death of a second child, in August 2025, also following an experimental treatment using a viral vector.

This time, the target was a different rare disease: Duchenne muscular dystrophy, caused by mutations in the DMD gene that result in little or no production of dystrophin, a protein essential for skeletal and cardiac muscle.

The experimental treatment, called HG302, had even received “orphan drug” designation from the FDA — a classification given to therapies intended for diseases with few or no available treatment options.

According to the company, the child who received a high dose of the treatment (and was the last participant enrolled in the study) developed acute respiratory distress syndrome, associated with strong activation of the complement system and cytokines (components of the immune system) after the viral vector was administered systemically, through the bloodstream rather than locally as in Mei’s case.

The pattern is repeating itself: once again, the cause of death appears to be linked to a severe immune reaction to the viral vector (the “vehicle” used to deliver the gene-editing instructions to cells).

It is the same type of vector (adeno-associated virus, or AAV) used in Mei’s case. This reinforces a concern raised by several experts: even though it is one of the most promising technologies in modern medicine, AAV-based gene therapy still faces an important obstacle: how the body responds to the massive doses of virus required to deliver the treatment.

According to HuidaGene, the other three participants in the study did not develop the same fatal syndrome and remain under long-term follow-up.

Before we wrap up and jump to conclusions, we need to take a breath.

We are not saying that gene therapy does not work or that it is inherently dangerous.

But, as with every scientific process, caution and rigor are essential to prevent tragedies like these from happening. That includes transparency in communication, rigorous review of data, and honesty about risks, especially when we are talking about human clinical trials and families who are desperate enough to risk everything for a cure.

Once again, our thoughts are with the families involved in both cases.

Until next time, scientists! 🧬

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How are you all doing? We’re bringing you some really exciting news!!

You probably remember that, during the pandemic, mRNA technology became part of everyday conversation because of the COVID-19 vaccines. Well, that same logic (giving the body instructions to produce a protein and thereby training the immune system) is now being tested, as we have discussed here yesterday, against a much older enemy: cancer.

And just last week, an important piece of news came out in this field.

Merck and Moderna announced that a Phase 3 study, called INTerpath-001, showed that an mRNA vaccine tailored to each individual patient, combined with an already approved immunotherapy (pembrolizumab, sold as Keytruda), significantly reduced the risk of melanoma coming back after surgery.

This is the first time that this type of therapy, called personalised neoantigen therapy, has shown a positive result in a Phase 3 trial.

Let’s understand what this actually means.

So, Scientist, let’s get into the science!!!

First of all, we need to understand why the immune system, on its own, often cannot handle cancer.

Unlike a virus, which is clearly “foreign” to the body, a tumour cell develops from our own cells. It only becomes dangerous because it accumulates mutations (changes in its genome). This means that, for the immune system to recognise the tumour as an enemy, it needs to learn to identify precisely those mutations, and every tumour has its own unique set of them.

This is where the central concept of the study comes in.

This image shows how neoantigens work. By developing a vaccine, we can increase recognition of these neoantigens and potentially fight melanoma.

And that is exactly what the therapy tested in this study does.

It is called intismeran autogene (also known as V940 or mRNA-4157), and it works like this:

When the vaccine is injected, the body’s cells “read” these instructions and begin displaying the neoantigens on their surface (almost as if they were putting up multiple WANTED posters at once). This attracts T cells, which learn to recognise and attack cells carrying those mutation patterns, including any remaining tumour cells that may have survived the surgery.

But the vaccine does not act alone in the study. It was tested in combination with pembrolizumab, a medication that is already a standard treatment for melanoma and works in a complementary way: it essentially “releases the brakes” on T cells, preventing the tumour from switching them off.

The idea is simple: the vaccine teaches the immune system what to target, while pembrolizumab makes sure the attack team doesn’t get blocked along the way.

And what were the results?

The study recruited 1,137 patients with advanced melanoma (stages IIB to IV) who had just undergone surgery to completely remove their tumours. Some received the vaccine + pembrolizumab combination, while others received pembrolizumab alone, which was already the standard treatment.

After following the patients, researchers found that the combination produced a statistically significant improvement in two outcomes: the time until cancer recurrence and the time until distant metastases developed.

In other words, the combination helped keep more patients disease-free for longer compared with the standard treatment alone.

It is worth remembering that this result had already been suggested in an earlier phase of the same research programme (Phase 2b), when the combination showed a substantial reduction in the risk of cancer recurrence.

Now, the Phase 3 trial — larger, more rigorous, and crucial for regulatory approval — has confirmed that benefit.

But, as alwaaaays:

Here are some important points to keep in mind before assuming this is “the cure for cancer”:

• First, these are preliminary topline results from an interim analysis. The complete data have not yet been published or peer-reviewed; they are expected to be presented at an international medical congress in the coming months.

• Second, a crucial endpoint, overall survival (in other words, whether patients actually live longer) is still being followed and has not been reported in this announcement.

• Third, this therapy is not yet approved for clinical use. The companies have announced that they will discuss the next steps with regulatory agencies, but that process can still take time.

And finally: this vaccine is custom-made, requiring genetic sequencing of each patient’s tumour and an individualised manufacturing process: something that is still expensive and logistically complex.

Expanding access to this type of therapy is a challenge of its own.

So, scientist? Did you learn something new?

Then subscribe to Eureka! and send this article to that friend who works in biotechnology — or who simply loves science!

Here we talk about science every day! Don’t miss out! :)

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You’ve definitely heard about mRNA vaccines during the pandemic. Pfizer, Moderna... Maybe you even remember that many people were suspicious of how quickly these vaccines were developed.

But what many people didn’t know is that this technology didn’t appear “out of nowhere.”

It had been studied for decades by scientists, including Katalin Karikó and Drew Weissman, who were awarded the 2023 Nobel Prize in Physiology or Medicine for fundamental work that helped transform mRNA into a viable vaccine platform.

And what if we told you that this same technology is now being used to try to teach the immune system to fight cancer?

That’s exactly what a group of researchers from BioNTech tested in this study published in Nature.

The scientists created personalised mRNA vaccines for patients with triple-negative breast cancer, one of the most aggressive forms of the disease. And the results are VERY interesting.

But first, if you want to become smarter and better informed and receive science every day, subscribe to Eureka!EN!!!!

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The idea

First, a few preliminary questions to help you understand today’s results!

→ What is messenger RNA (mRNA), and how does an mRNA-based vaccine work?
→ And perhaps the most important question: how do you get the immune system to attack something as complicated as cancer, which arises from our own cells?

Let’s take it step by step!

First, let’s talk about this thing called mRNA.

One of the most important ideas in modern biology is the so-called Central Dogma of Molecular Biology. You’ve probably heard about how important proteins are in your body. And we’re not just talking about whey protein 😅

Proteins are the great “molecular machines” of life. They participate in practically everything: digestion, movement, cell signalling, immune defence, molecular transport… But proteins need to be produced according to instructions. Those instructions are stored in DNA.

The thing is, cells don’t normally carry the entire DNA molecule to the place where proteins are produced. Instead, they create a temporary copy of the recipe. That copy is messenger RNA, or mRNA.

DNA stores the information. RNA transports that information. And proteins perform functions in the body.

mRNA vaccines

And here comes the genius of mRNA vaccines: instead of injecting dead or weakened viruses, or pieces of viruses, scientists simply deliver the instructions. The vaccine sends mRNA molecules into our cells, and they temporarily start producing a specific viral protein.

In the case of COVID, for example, that famous protein is the Spike protein.

After that, the mRNA is naturally degraded by the body within a relatively short period of time. It does not alter your DNA and does not remain permanently in the body (watch out for the fake news, Scientist!).

The immune system sees the protein, recognises it as foreign, and learns to recognise it.

Cancer vaccines

Perhaps the biggest challenge in treating cancer is precisely this: cancer develops from our own “healthy” cells. This makes it much harder for the immune system to distinguish tumour tissue from normal tissue.

But tumour cells accumulate mutations. And mutations alter proteins. These altered proteins can generate small fragments called neoantigens (we have covered this before in a previous Eureka Concept).

And these neoantigens can function almost like the tumour’s “fingerprints.”

Now we can finally talk about what the scientists actually did — and, spoiler alert, it was incredibly ingenious!

The idea was to teach T cells in the immune system to recognise those mutations and attack cancer cells carrying them.

And the results are striking. In practically all of the patients, the vaccine generated strong T-cell responses against multiple tumour neoantigens.

But it wasn’t just a temporary response. Some of those immune cells remained detectable for YEARS.

The researchers followed patients for up to 6 years and found T cells still circulating and functioning.

That is VERY positive. Because one of the major problems with cancer is recurrence. Sometimes treatment eliminates almost everything… except a few hidden cells. And years later, they come back.

Triple-negative breast cancer is particularly known for aggressive recurrences, especially during the first few years after treatment.

In the study, 11 of the 14 patients remained recurrence-free for up to six years after vaccination.

But the data suggest something extremely promising: perhaps it is possible to create long-lasting immune memory against tumour-specific mutations.

And here comes a fascinating part:

The researchers observed two major groups of T cells emerging after vaccination:

• cells already prepared to attack immediately
• cells with a memory profile, capable of persisting and renewing themselves over long periods

It’s almost as if the body had created both active soldiers and a strategic reserve.

But the study also showed the limitations of this strategy.

In one patient, the tumour apparently escaped by reducing molecules used by cells to “display” fragments to the immune system. In other words: the cancer seemed to try to hide its identity from the immune system.

And that’s important because it helps scientists understand how tumours evolve to escape immune-based therapies.

The average manufacturing time was around 69 days! This is personalised medicine at a VERY advanced level!!

Perhaps we are beginning to enter an era in which treatments will be created specifically for the mutations found in each person’s tumour.

Pretty cool, right?

It’s pretty surreal to think that the same technology many people first encountered during the pandemic may now be helping researchers develop new ways to fight cancer.

Did you enjoy spending a few minutes of your morning learning some molecular biology and discovering research that could change the future of cancer treatment? Then subscribe to Eureka! and have coffee with science every day! ☕🧬

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And if this news impressed you, share it with someone who loves science, medicine, or biology!

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Skin cancer is one of those topics that never goes out of style, so today we're talking about one of the most important forms of it: melanoma.

Your skin is the largest organ in your body, covering roughly 2 square meters (about 22 square feet). Like every other organ, it deserves regular care and attention. Melanoma is an aggressive form of skin cancer that develops from melanocytes, the cells responsible for producing melanin, which is the pigment that gives color to your skin, hair, and eyes.

Skin Cancers: Carcinoma & Melanoma – Health Journal.

Melanin helps protect cellular DNA from ultraviolet (UV) radiation by acting as the skin’s natural sunscreen, absorbing part of the incoming UV light.

Although melanoma accounts for only 1–5% of all skin cancers, it causes the majority of skin cancer deaths because of its high potential to spread (metastasize) to other organs.

Melanoma is more common among people with lighter skin tones. Lifetime risk is estimated at around 3% in White individuals, compared with approximately 0.1% in Black individuals.

But here’s an important point:

Lower risk does not mean zero risk.

Melanoma can develop in people of every skin tone, including Black, Brown, and olive skin. In individuals with darker skin, melanoma is often diagnosed later because many people don’t expect it to occur in these populations. Another important detail is that it frequently appears in areas with little or no sun exposure, including the palms of the hands, soles of the feet, beneath the nails, inside the mouth, and in the genital or anal regions.

The average age at diagnosis is around 67 years, although melanoma is also one of the most common cancers in young adults, particularly women.

According to the International Agency for Research on Cancer (IARC/WHO), excessive ultraviolet (UV) exposure is the most important preventable risk factor and is responsible for approximately 83% of melanoma cases worldwide.

Illustration showing the layers of the skin and where melanoma develops.

So how can I recognize melanoma early?

Don’t worry, that’s exactly what today’s article is about.

Let’s talk about one of the most useful tools for early detection: the ABCDE rule.

Regular skin self-examinations are an important preventive measure and should ideally be performed once a month. To do a thorough self-exam, stand in a well-lit room with both a full-length mirror and a handheld mirror so you can inspect hard-to-see areas.

Work through your body systematically. Start with your face, ears, neck, chest, and abdomen. Then examine your underarms, both sides of your arms, your hands, between your fingers, and underneath your fingernails. Use the handheld mirror to inspect your neck, back, buttocks, and the backs of your legs. Finally, sit down to examine the fronts of your legs, your feet, the spaces between your toes, and the soles of your feet. Using a comb or hair dryer can help you inspect your scalp.

As you examine each mole or spot, apply the ABCDE rule:

A – Asymmetry: one half doesn’t match the other.

B – Border: irregular, blurred, or poorly defined edges.

C – Color: multiple colors or uneven pigmentation within the same lesion.

D – Diameter: larger than about 6 mm (roughly the size of a pencil eraser).

E – Evolving: any change in size, shape, or color over time.

Among these, E for Evolution is considered one of the most important warning signs, because change over time is often more concerning than any single feature alone.

Also watch for sores that don’t heal, spots that itch, hurt, or bleed, and any new mole that looks noticeably different from the others> the so-called “ugly duckling” sign.

Keeping photographs or notes of your moles can help you notice subtle changes over time. Any suspicious change should be evaluated promptly by a dermatologist, who is the healthcare professional best qualified to diagnose skin cancer.

Can melanoma be prevented?

Absolutely. Here are the main recommendations:

• Avoid prolonged sun exposure during peak UV hours, generally between 10 a.m. and 4 p.m.

• Wear protective clothing, including wide-brimmed hats, UV-protective sunglasses, and garments that cover exposed skin.

• Apply a broad-spectrum sunscreen with SPF 30 or higher (SPF 50+ for prolonged outdoor exposure), and reapply every two hours—or sooner after swimming or heavy sweating.

• Avoid indoor tanning beds. They are classified by the World Health Organization as Group 1 carcinogens, meaning there is sufficient evidence that they cause cancer.

Life advice: don’t be the person defending indoor tanning.

One final takeaway

Schedule a yearly skin examination with a dermatologist, especially if you notice any mole or spot that meets the ABCDE criteria.

Only a trained professional can accurately diagnose—or rule out—melanoma.

Following these recommendations can substantially reduce your risk of developing skin cancer.

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See you tomorrow for another fresh serving of science! Hot, just like your morning coffee. ☕🔬

There has been a remarkable mobilization involving science communicators, public figures, and even some public institutions to try to help Lito, a Brazilian entrepreneur and aviator diagnosed with Creutzfeldt-Jakob disease (CJD), gain access to one of the ongoing clinical trials evaluating new therapies for this devastating disease. The movement reflects both the aggressive nature of CJD and the fact that no treatment is currently available to slow its progression.

The entire Eureka!EN team stands with Lito and his family during this incredibly difficult time. We’re all hoping for the best.🙏🏻

Yesterday we published an introductory article explaining what Creutzfeldt-Jakob disease is and why it remains incurable. If you haven't read it yet, we recommend starting there and then coming back to this article.

Currently, two important clinical trials are underway. They’re worth discussing, not only because of the hope they represent, but also because there’s been a lot of confusion surrounding them.

Before we begin, if you’re new here, subscribe to Eureka!EN Free science, delivered to your inbox every day.

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The idea behind both trials

As we explained yesterday, the disease develops because an abnormally folded prion protein causes nearby normal prion proteins to adopt the same abnormal shape, creating a domino effect that ultimately destroys neurons.

Nature.

That leads to a simple but powerful idea:

If there were fewer normal prion proteins available, there would be fewer dominoes left to fall.

Previous approaches, including quinacrine, doxycycline, pentosan polysulfate, and monoclonal antibodies, attempted to destroy or neutralize the already misfolded protein. None demonstrated clear clinical benefit.

The current strategy turns that idea upside down.

Instead of targeting the abnormal protein, researchers are trying to reduce production of the normal protein before it can become misfolded.

A 2008 study had already demonstrated that RNA interference could reduce prion protein production.

This strategy is supported by two important observations: in animal models, lowering PrP levels delays disease onset and slows disease progression. In addition, organisms that naturally produce lower levels of this protein appear to live normally, suggesting that targeting PrP may be relatively safe.

Suggesting is the key word.

Testing whether this is truly safe and effective in humans is exactly what these new trials are beginning to do.

From DNA to protein 🧠

Every protein in your body starts as a gene: a segment of DNA stored inside the cell nucleus. That original blueprint never leaves the nucleus. When a cell needs to make a protein, it creates a working copy called messenger RNA (mRNA). This copy travels outside the nucleus to the cellular machinery responsible for assembling the protein, one amino acid at a time.

In other words:

For CJD, the gene is PRNP, and the final protein produced is PrP, the prion protein.

Both experimental treatments act in the middle of this pathway, targeting the messenger RNA.

The two clinical trials

How the drug works

ION717 is an antisense oligonucleotide (ASO), a short synthetic strand designed to perfectly match the messenger RNA that carries instructions for making PrP. When injected into the cerebrospinal fluid, it spreads through the central nervous system and binds specifically to that RNA, almost like molecular Velcro.

Once attached, the RNA is recognized by one of the cell’s own enzymes, which destroys the messenger RNA. Without the RNA blueprint, the cell can no longer manufacture the prion protein. Because the drug is gradually cleared from the body, repeated dosing is required.

Study design

This is a Phase 1/2a, multicenter, randomized, double-blind clinical trial conducted at approximately 13 centers. It enrolled 56 symptomatic patients during 2024.

Current status

Preliminary data suggest an acceptable safety profile. However, the reduction in prion protein levels was smaller than expected. As a result, the company added a third, higher-dose treatment group in 2026, extending the trial through 2027.

How this drug works

PRiSM evaluates a small interfering RNA (siRNA) therapy. Like the ASO, it binds specifically to the messenger RNA that codes for PrP. The difference comes afterward.

Instead of simply marking the RNA for destruction, the siRNA becomes part of a naturally occurring cellular complex known as RISC, which functions like a molecular pair of scissors. The siRNA serves as a guide, directing this molecular machinery to the correct RNA molecule, which is then cut into pieces. One advantage is that the scissors aren’t consumed during the process: they can continue destroying additional RNA molecules.

The drug being tested is also a divalent siRNA, meaning it contains two chemically linked siRNA molecules designed to improve distribution throughout the brain and prolong its activity. Because of this design, researchers hope a single dose may produce a long-lasting effect.

Study design

This is a first-in-human Phase 1 trial evaluating a single dose. Recruitment began in April 2026 and includes only patients with confirmed symptomatic disease. The primary goals are to evaluate safety and determine whether the treatment reduces detectable PrP levels in cerebrospinal fluid.

Who is leading the study?

The principal investigator is Eric Minikel, one half of the couple we mentioned yesterday. In 2011, he and his wife, Sonia Vallabh, dramatically changed their careers after Sonia learned she had inherited the fatal PRNP mutation.

The drug now entering clinical trials was developed in their laboratory. Fifteen years after making that life-changing decision, their work has finally reached patients.

What does “Phase 1” actually mean?

A Phase 1 clinical trial is an early-stage study whose primary goal is to evaluate safety and appropriate dosing. Even if the results are encouraging, the treatment must still go through additional clinical testing before it can be approved.

Does this mean mRNA COVID vaccines cause Creutzfeldt-Jakob disease?

No.

It’s important to understand where this misconception comes from:

mRNA vaccines deliver instructions for cells to temporarily produce one specific viral protein (the coronavirus spike protein), allowing the immune system to learn to recognize it. That mRNA naturally degrades within days and never enters the cell nucleus.

The experimental CJD treatments do the opposite: instead of instructing cells to make a protein, they block the production of an entirely different protein (the prion protein - PrP) by preventing its messenger RNA from being used.

Neither approach interacts with the PRNP gene itself.

A recent Canadian study analyzing national CJD surveillance data from 2016 to 2025 found that the incidence of Creutzfeldt-Jakob disease remained stable throughout and after the COVID-19 pandemic, with no association between COVID-19 and CJD.

Prion diseases are closely monitored worldwide because they are extremely rare. Any meaningful increase would almost certainly have been detected.

The real challenges of joining a clinical trial

This part is rarely discussed, but it’s extremely important.

Eligibility criteria are strict.

Each trial specifies detailed requirements regarding age, disease stage, previous testing, medical conditions, and many other factors. Many patients are excluded for reasons entirely unrelated to their desire to participate.

Time is another major obstacle. For a disease with a median survival of only four to six months, delays between diagnosis, referral, screening, and enrollment can make participation impossible.

Finally, enrollment decisions are not made by patients or by the sponsoring companies. They are made independently by the investigators at each study site. Sponsors cannot intervene in decisions regarding individual patients.

An important issue of equity

Notice where these studies are taking place: The United States, Germany, and France.

None are located in Latin America.

Clinical research remains heavily concentrated in high-income countries, and even within those countries, participation is not equally distributed.

In the United States, for example, people of Hispanic or Latino origin represent about 19% of the population, yet historically account for a much smaller proportion of clinical trial participants.

Similar disparities exist for Black and Indigenous populations.

The reasons are well known: language barriers, distance from research centers, indirect costs, lack of health insurance, immigration concerns, fewer referrals from healthcare providers, and eligibility criteria that disproportionately exclude people with poorly controlled chronic illnesses.

This isn’t just an issue of fairness, although that alone would be reason enough.

It’s also a scientific problem.

Responses to medications may vary according to genetic ancestry.

In prion diseases specifically, variation in the PRNP codon 129 polymorphism influences both susceptibility and disease presentation, and the frequency of this genetic variant differs among populations.

Testing a treatment in only a narrow segment of the population means learning less about how it may perform in everyone else.

Had you ever stopped to think about how the geography of clinical research influences who gets access to experimental treatments?

Let us know what you think in the comments. And share this article with someone you think should read this!

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See you tomorrow for more science!

Many of you may have seen the sad news that Lito Sousa, aviation expert and creator of the popular aviation channel Airplanes and Music, has been diagnosed with the rare neurological disorder Creutzfeldt–Jakob disease (CJD). The diagnosis was announced by his wife, entrepreneur Mila Seidl, after several weeks of neurological investigation.

Before anything else, it’s important to respect Lito and his family during this incredibly difficult time. Diagnoses like this are devastating, and speculation or insensitive comments on social media only add to the burden they’re already carrying.

New England Journal of Medicine

Today’s article explains why this disease is so important from a scientific perspective. We’ll explore what CJD is, why there is still no cure, what researchers have tried so far, the warning signs to recognize, and whether you should be concerned.

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First things first: how do you pronounce it?

The names are German, and the English pronunciation is approximately:

“KROYTS-felt YAH-kob.”

The disease is named after two German physicians who described the first reported cases in the early 1920s: Hans Gerhard Creutzfeldt and Alfons Maria Jakob. Interestingly, later reviews suggest that the original case described by Creutzfeldt probably wasn’t actually the disease that now bears his name.

The discovery that nearly destroyed a scientist’s career

In the 1950s, American physician Carleton Gajdusek traveled to Papua New Guinea to investigate a mysterious illness affecting the Fore people. They called it kuru, meaning “trembling.” The disease caused loss of coordination, tremors, and eventually death, primarily affecting women and children.

Carleton Gajdusek in Papua New Guinea. Source: NIH

Gajdusek discovered that the disease was linked to ritual funerary cannibalism, during which the brains and internal organs of deceased relatives were consumed. Once the practice ended, kuru disappeared. His work earned him the 1976 Nobel Prize in Physiology or Medicine.

But one mystery remained: what exactly was being transmitted?

Researchers couldn’t find any virus, bacterium, or parasite.

Then, in the 1980s, neurologist Stanley Prusiner at the University of California, San Francisco proposed something revolutionary: the infectious agent was a protein. He introduced the term prion in 1982.

At the time, this idea challenged one of biology’s central dogmas. How could something without DNA or RNA reproduce? Many scientists dismissed the concept. Fifteen years later, in 1997, Prusiner received the Nobel Prize for proving they were real.

Source: PNAS

How prions work: a molecular domino effect

Every one of us naturally produces a protein called PrP (prion protein) on the surface of our cells, especially neurons. Under normal circumstances, this protein is harmless.

The disease begins when one prion protein folds into the wrong shape. That abnormal protein then forces nearby normal proteins to adopt the same abnormal structure. One misfolded protein changes two. Those two change four. The process becomes a self-amplifying chain reaction.

These misfolded proteins accumulate into aggregates that neurons cannot eliminate. As neurons die, tiny holes appear throughout the brain tissue, giving it a sponge-like appearance.

Source: Nature Reviews Disease Primers

Why is there still no cure?

The immune system doesn’t recognize prions as foreign because they closely resemble the body’s own proteins. To make matters worse, prions are extraordinarily resistant. They survive boiling, alcohol, formaldehyde, ultraviolet light, ionizing radiation, and standard hospital sterilization procedures. Proper inactivation requires concentrated sodium hydroxide or prolonged autoclaving at 134°C (273°F).

Once symptoms begin, the median survival is only four to six months, and approximately 90% of patients die within one year.

Because the disease affects only one to two people per million each year, conducting adequately powered clinical trials is extremely challenging.

What treatments have been tested?

Researchers have evaluated numerous potential therapies over the years:

• Quinacrine, an old antimalarial drug, showed excellent results in laboratory cell cultures but ultimately failed to improve survival in the PRION-1 clinical trial.

• Pentosan polysulfate, delivered directly into the brain’s ventricles, produced encouraging case reports but has never demonstrated benefit in controlled studies.

• Doxycycline was also tested in randomized clinical trials without success.

• Flupirtine showed modest cognitive improvements in a small German study but did not extend survival.

• A monoclonal antibody called PRN100, developed at University College London, became the first antibody therapy administered to humans with prion disease. It successfully reached the brain and engaged its target but did not demonstrate clear clinical benefit.

• More recently, ION717, an antisense oligonucleotide (ASO) developed by Ionis Pharmaceuticals, has taken a different approach. Rather than targeting abnormal prions directly, it reduces production of the normal prion protein itself.

Early results from the ongoing PrProfile trial have shown encouraging safety data, although the reduction in prion protein levels has been smaller than expected. The trial has therefore been expanded to include a higher-dose treatment group.

Meanwhile, a 2025 Nature Medicine study demonstrated that gene editing significantly extended survival in humanized mouse models of prion disease, offering hope that future therapies may eventually become possible.

The three forms of Creutzfeldt–Jakob disease

There are three major forms of CJD.

• Sporadic CJD (85–90% of cases) develops without any identifiable cause. The prion protein simply misfolds spontaneously. It is not inherited, not contagious through everyday contact, and not caused by anything the patient did. This is the most common form, and likely the diagnosis reported in the recent news.

• Genetic CJD (10–15%) results from inherited mutations in the PRNP gene.

• Acquired CJD (less than 1%) includes the variant associated with contaminated beef during the “mad cow disease” outbreak in the United Kingdom during the 1990s, as well as extremely rare cases transmitted through certain medical procedures.

  ---

Warning signs

Typical symptoms include rapidly progressive cognitive decline, sudden involuntary muscle jerks (myoclonus), loss of coordination, visual disturbances, and behavioral or psychiatric changes such as apathy, anxiety, depression, or personality changes.

In advanced stages, patients may develop akinetic mutism, losing the ability to move and speak.

One particularly important point (also seen in Lito’s case) is that the condition initially can resemble autoimmune encephalitis.

This isn’t unusual.

Rapidly progressive dementia has many possible causes, and some of them are treatable, including autoimmune encephalitis, infections, vitamin B12 deficiency, thyroid disorders, medication side effects, and certain brain tumors.

Today, diagnosis relies on a combination of clinical evaluation, brain MRI (particularly diffusion-weighted imaging), EEG, and cerebrospinal fluid testing. Definitive confirmation still requires examination of brain tissue.

Please choose kindness in what you comment, share, and speculate about online.

Our thoughts are with Lito, Mila, and everyone close to them. ❤️🧬

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If you found today’s article helpful, share it with someone who may have questions about Creutzfeldt–Jakob disease.

Good information remains the best antidote to misinformation.

See you tomorrow with more science. 🔬

References:

• Prusiner SB. Novel proteinaceous infectious particles cause scrapie. Science. 1982;216:136-144.

• Mead S, Khalili-Shirazi A, Potter C, et al. Prion protein monoclonal antibody (PRN100) therapy for Creutzfeldt-Jakob disease: evaluation of a first-in-human treatment programme. Lancet Neurol. 2022;21:342-354.

• Ionis Pharmaceuticals. PrProfile: A Study to Assess the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of ION717. ClinicalTrials.gov NCT06153966.

• An M, Davis JR, Levy JM, et al. In vivo base editing extends lifespan of a humanized mouse model of prion disease. Nat Med. 2025;31:1319-1328.

Today we’re covering an important topic: the growing incidence of pancreatic cancer among younger adults and two promising therapies currently under investigation.

By the end of this article, you’ll understand which symptoms deserve medical attention and who is at greater risk of developing this disease.

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Let’s dive in!

Image source: News-Medical.net.

A Changing Patient Profile

Although most pancreatic cancer diagnoses still occur after the age of 55, a study published in JCO Global Oncology suggests that both the incidence and mortality of pancreatic cancer in adults aged 49 years or younger are expected to increase over the coming decades.

The analysis used data from the Global Burden of Disease project, which compiles health information from 204 countries, and suggests that early-onset pancreatic cancer could become one of the world’s major public health challenges by 2040.

Why Is Pancreatic Cancer Often Diagnosed So Late?

One of the greatest challenges is that pancreatic cancer is often silent during its early stages. In most patients, routine tests such as blood work or abdominal ultrasound fail to detect the disease. By the time symptoms appear, the cancer has frequently reached an advanced stage, limiting treatment options and worsening prognosis.

According to a 2025 clinical review published in The Lancet, approximately 80% of cases are diagnosed at an advanced stage, and only about 15% of patients survive five years after diagnosis.

When Should You Seek Medical Attention?

The symptoms of pancreatic cancer are not specific, meaning they can also occur in many other, much more common conditions. However, when they persist, especially in people with risk factors, they deserve medical evaluation.

One of the most recognizable signs is jaundice, a yellow discoloration of the skin and eyes that may occur when the tumor blocks the bile duct.

Image source: GoodRx.

Persistent pain in the upper abdomen that radiates to the back may also occur. Other possible symptoms include unexplained weight loss, loss of appetite, nausea, vomiting, and pale or greasy stools. A lesser-known but increasingly recognized warning sign is new-onset diabetes after the age of 40 or 50.

A study published in JAMA Oncology estimated that approximately 1% of new diagnoses of type 2 diabetes in this age group may actually be caused by an underlying pancreatic tumor.

Who Is at Higher Risk?

Several factors increase the likelihood of developing pancreatic cancer.

Age remains one of the strongest risk factors, with incidence increasing substantially after age 60.

Promising New Treatment Options

A Phase II clinical trial, published in Nature Medicine in 2026, evaluated a new first-line treatment strategy for metastatic pancreatic cancer. Researchers tested elraglusib, an inhibitor of the GSK-3β protein, in combination with standard chemotherapy (gemcitabine plus nab-paclitaxel), comparing it with chemotherapy alone. The international multicenter trial enrolled 233 patients.

Image source: Selleck Chemicals.

The results showed that patients receiving elraglusib experienced an approximately three-month improvement in median overall survival, along with a 38% reduction in the risk of death. One-year survival reached 44%, compared with 22% in the control group.

Although these findings are promising, they still require confirmation in larger studies.

Another Exciting Development

Biotechnology company Revolution Medicines recently announced the first results from its Phase III clinical trial evaluating daraxonrasib.

The findings attracted considerable attention within the oncology community. Among one subgroup of patients, median overall survival reached 13.2 months, compared with 6.7 months in those receiving standard chemotherapy. According to data reported by STAT News, the treatment reduced the risk of death by approximately 60%.

Image source: STAT News.

This result is particularly noteworthy because the drug targets the RAS signaling pathway, which is altered in more than 90% of pancreatic cancers and has remained one of the most difficult targets in cancer drug development for decades.

When mutated, the RAS gene promotes uncontrolled cell growth and survival. Developing drugs against this pathway has historically been extremely challenging because the RAS protein has a very smooth molecular surface, leaving few places for medications to bind effectively.

Daraxonrasib is taken as a once-daily oral tablet. One widely publicized participant in the clinical trial was Ben Sasse, the former U.S. senator, whose tumors reportedly shrank by 76% after treatment.

Image source: CNBC.

The drug has not yet received FDA approval, and additional studies are still needed before it becomes available for routine clinical use.

What Does This Mean in Practice?

Neither of these therapies has been approved for routine clinical use yet.

Key Takeaways

Pancreatic cancer often develops silently, making early diagnosis particularly difficult. At the same time, the disease appears to be becoming more common in adults under the age of 50.

Persistent jaundice, upper abdominal pain that radiates to the back, unexplained weight loss, persistent nausea or vomiting, pale or greasy stools, and new-onset diabetes after age 40 or 50 may all warrant medical evaluation, particularly when multiple symptoms occur together.

The major risk factors include smoking, obesity, frequent alcohol consumption, chronic pancreatitis, long-standing type 2 diabetes, a family history of pancreatic cancer, and inherited BRCA1 or BRCA2 mutations.

While promising new therapies are emerging, early recognition of symptoms and risk factors remains one of the most important tools we have today.

Thank you for reading!

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Today we’re talking about loneliness—a condition that affects one in six people worldwide and has a measurable impact on health.

Two recent publications have placed this topic at the center of scientific discussion. One is the largest report ever produced on the subject, published by the World Health Organization (WHO) in 2025. The other is a meta-analysis of 90 studies involving more than 2.2 million people, published in Nature Human Behaviour in 2026.

Together, they suggest that loneliness has important health consequences that deserve much more attention.

The World Health Organization warns about the health risks of loneliness

In June 2025, the World Health Organization released the most comprehensive report ever published on social connection, bringing together data from dozens of countries and millions of people.

Its main conclusion was clear:

These findings were reinforced by the 2026 meta-analysis published in Nature Human Behaviour, which reported that:

Both social isolation and loneliness are also associated with a higher risk of cardiovascular disease (around 29%) and stroke (approximately 32%). Among older adults, they are linked to up to a 50% higher risk of dementia.

How does loneliness affect the body?

One of the leading hypotheses involves chronic low-grade inflammation. In this state, the immune system remains persistently activated, even when there is no real threat. Over time, this ongoing inflammatory response may damage the cardiovascular system and other organs, potentially contributing to the development of chronic diseases.

When the brain perceives prolonged social isolation, it may interpret it as a threat to survival. In response, it activates the body’s stress system by increasing cortisol production, raising blood pressure, and maintaining a chronic inflammatory state.

This may help explain why long-term loneliness has been associated with so many adverse health outcomes.

Who is most at risk?

Here’s a finding that challenges a common misconception.

Most people assume loneliness mainly affects older adults.

The data suggest otherwise.

In low-income countries, loneliness rates are roughly twice as high as those reported in high-income countries (24% versus 11%).

Although patterns vary across countries and cultures, increasing urbanization, social isolation, and excessive social media use have become growing concerns in many parts of the world, particularly since the COVID-19 pandemic.

What can we apply to our own lives? ☕

The encouraging news is that social connection, much like physical exercise, appears to have a dose-response effect: every improvement counts!

Making time for friends and family, prioritizing in-person interactions whenever possible, participating in regular group activities, and maintaining meaningful social routines can all help strengthen social connection.

If you notice yourself becoming increasingly isolated, it’s worth treating that as seriously as you would any other warning sign from your body. And if feelings of loneliness are accompanied by persistent sadness or depression, seeking professional support can make an important difference.

One final thought

Research on loneliness is still evolving, but the evidence accumulated so far is enough to suggest that social connection deserves to be considered alongside healthy eating, regular exercise, and good sleep as a pillar of long-term health.

Loneliness is not a sign of weakness. It is a common human experience—and one that can be addressed.

If you or someone you know has been struggling with persistent loneliness or emotional distress, reaching out to a trusted healthcare professional or a local mental health support service can be an important first step.

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Thank you for reading, and we’ll see you tomorrow with more science! 🔬

One of the things we love most at Eureka!EN is following the latest scientific discoveries that have the potential to transform medicine.

Today, we’ve selected three recent advances that could have a meaningful impact on human health. From gene editing for sickle cell disease to a promising new treatment for blood cancer (and an intriguing finding about influenza vaccination) you won’t want to miss these.

If you’re new here, don’t forget to subscribe to Eureka!EN. We bring evidence-based science straight to your inbox every day.

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Now, let’s dive in!

1. Could We Correct the Gene Behind Sickle Cell Disease?

Scientist, have you ever heard of sickle cell disease?

Sickle cell disease is an inherited disorder that affects millions of people worldwide. Individuals with the condition carry a mutation in the hemoglobin gene, causing their red blood cells to become sickle-shaped. These abnormal cells can clog blood vessels, leading to severe pain crises, chronic anemia, and damage to multiple organs.

Until recently, the only potentially curative treatment was a bone marrow transplant, which requires a compatible donor and carries significant risks.

However, a study published in April 2026 in the New England Journal of Medicine, one of the world’s most prestigious medical journals, may offer a promising new therapeutic approach.

Researchers used a technique known as base editing: think of it as a molecular “correction pen” to modify each patient’s own hematopoietic stem cells outside the body before reinfusing them.

Their goal was to switch fetal hemoglobin (HbF) production back on. Although our bodies naturally stop producing fetal hemoglobin shortly after birth, reactivating it allows red blood cells to function much more normally despite the sickle cell mutation.

In other words, the edited cells receive a new instruction:

The early results were encouraging

Among the 31 patients included in the study, more than 60% of their hemoglobin consisted of fetal hemoglobin six months after treatment, while sickle hemoglobin accounted for less than 40%.

These are very promising findings. That said, it’s important to keep the results in perspective.

This was still a Phase 1–2 clinical trial, designed primarily to evaluate safety and generate initial evidence of effectiveness. The study included relatively few participants and only short-term follow-up. One participant died from treatment-related complications, highlighting that important safety questions remain unanswered.

Although much more research is needed before this approach becomes widely available, it represents an exciting step forward in the treatment of sickle cell disease.

2. A New Drug Combination for Multiple Myeloma

Multiple myeloma is a cancer of plasma cells—the immune cells responsible for producing antibodies. It is the second most common blood cancer worldwide, and despite major advances in recent years, it is still considered incurable in most patients.

Standard treatment typically involves chemotherapy followed by an autologous stem cell transplant. One of the biggest questions researchers are trying to answer today is:

A study published in April 2026 in Nature Medicine set out to answer exactly that.

Researchers randomized 302 patients with newly diagnosed multiple myeloma into two treatment groups. One group received a four-drug combination (isatuximab + carfilzomib + lenalidomide + dexamethasone), while the other received the same regimen without isatuximab.

Isatuximab is a monoclonal antibody that specifically targets myeloma cells.

The primary endpoint was minimal residual disease (MRD) negativity—in other words, whether any cancer cells could still be detected after treatment, even at extremely low levels.

The results showed that patients receiving the four-drug regimen achieved significantly higher MRD negativity rates: 77% versus 67% in one analysis, and 68% versus 48% using an even more sensitive assessment method. Importantly, the safety profile was similar between the two groups.

We still don’t know whether these laboratory improvements will ultimately translate into longer progression-free survival or improved overall survival. Nevertheless, these findings suggest that the four-drug regimen could become a strong candidate for a new standard of care.

3. Could a High-Dose Influenza Vaccine Reduce the Risk of Alzheimer’s Disease?

Alzheimer’s disease remains one of the most feared conditions associated with aging, and unfortunately, we still do not have a cure. For that reason, any strategy that might help prevent or delay its onset attracts considerable scientific attention. One area of growing interest is the possible relationship between vaccination and protection against dementia.

MedlinePlus.

An observational study published in the journal Neurology investigated whether receiving a high-dose influenza vaccine was associated with a lower risk of developing Alzheimer’s disease compared with the standard-dose vaccine.

Researchers analyzed health records from more than 120,000 adults aged 65 years and older in the United States and followed them for up to three years.

The findings were encouraging. People who received the high-dose influenza vaccine had a lower risk of developing Alzheimer’s disease during the first 25 months of follow-up compared with those who received the standard-dose vaccine. Interestingly, the protective association appeared to be stronger and longer-lasting in women than in men.

One possible explanation is that vaccination reduces systemic inflammation or stimulates the immune system in ways that may also benefit the brain. However, the biological mechanisms remain uncertain.

It’s important to remember that this was an observational study, not a randomized clinical trial. That means the study can identify an association but cannot prove causation, something we always like to emphasize here at Eureka!

It also remains unclear whether the observed effect results from better protection against influenza itself or from other immune-related mechanisms. In addition, the follow-up period was relatively short for a disease that develops over decades.

Still, given that participants were approximately 65 years or older, even an early signal of benefit is encouraging.

It’s also worth noting that these findings are not isolated. Previous studies—including a recent meta-analysis—have reported that influenza vaccination, even at the standard dose, is associated with approximately a 13% lower risk of dementia.

Science Never Stops Moving!!

From gene editing to cancer therapies and Alzheimer’s prevention, these studies highlight how quickly biomedical research continues to evolve.

Some discoveries may eventually transform clinical practice. Others still require years of additional research before becoming part of routine medical care.

That’s exactly why we love following science: it is always moving forward!!

If you enjoyed today’s roundup, share it with someone who loves science (or someone who thinks nothing exciting ever happens in research!).

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See you tomorrow with more science! 🧬

Before we dive into today’s article, here’s a quick question:

Give your vote above before reading on!

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And since we’re talking about high blood pressure: do you or any member of your family have this condition?

Source: biologyofhumanaging.com

According to the World Health Organization, more than 1 billion people worldwide are living with hypertension.

Most people know that exercise helps lower blood pressure.

What far fewer people know is which type of exercise appears to work best.

The largest study ever conducted on exercise and blood pressure

Researchers from Canterbury Christ Church University (UK) analyzed 270 randomized controlled trials published between 1990 and 2023, including a total of 15,827 participants.

They compared five different categories of exercise:

• Aerobic exercise (walking, running, cycling)

• Traditional resistance training

• Combined training (aerobic plus resistance)

• High-intensity interval training (HIIT)

• Isometric exercise

The results, published in the British Journal of Sports Medicine, showed one clear winner:

Isometric exercise.

By a considerable margin.

But what exactly is isometric exercise?

Eureka Concept 🧠

Isometric exercise involves contracting a muscle without moving the joint. Instead of lifting or lowering a weight, you simply hold a position under tension.

Classic examples include the wall sit, the plank, and handgrip exercises

.

The numbers that surprised researchers

The average reduction in systolic blood pressure (the top number in a blood pressure reading) was:

• Aerobic exercise: 4.49 mmHg

• Resistance training: 4.55 mmHg

• HIIT: 4.08 mmHg

• Combined training: 6.04 mmHg

• Isometric exercise: 8.24 mmHg

The important takeaway is that every form of exercise lowered blood pressure—and the reductions were both statistically and clinically significant.

However, isometric exercise nearly doubled the blood pressure reduction seen with most other exercise modalities.

When researchers looked more closely at specific isometric exercises, the wall sit produced the largest effect, reducing systolic blood pressure by 10.47 mmHg and diastolic blood pressure by 5.33 mmHg.

The authors even noted that this magnitude of improvement is comparable to what is often achieved with a standard antihypertensive medication.

That certainly doesn’t mean people should stop taking their medication—it simply highlights how powerful regular physical activity can be.

Researchers believe these effects may result from improvements in endothelial function and reductions in peripheral vascular resistance.

A simple protocol used in several studies

Wall sit demonstration.

One of the protocols frequently used in the studies was remarkably simple:

Hold a wall sit for two minutes, rest for one to two minutes, and repeat this cycle four times.

Including the rest periods, the entire session takes about 14 minutes.

Participants performed the routine three times per week.

If you’ve never tried wall sits before, start with 20 to 30 seconds and gradually build your endurance.

Don’t be surprised if your legs start shaking near the end—that’s completely normal.

Should I stop running or walking and only do isometric exercises?

Not at all!!

The researchers themselves emphasized that any exercise is beneficial.

Their message was simple:

If you’re already exercising regularly but your blood pressure remains difficult to control, adding isometric exercise may provide additional benefits.

The goal isn’t to replace the activities you already enjoy.

It’s to complement them.

What can you apply to your daily routine?

If you’re interested in trying isometric exercise, a practical starting point is a few short wall sits several times per week, gradually increasing the duration as you become stronger.

The exercise requires no gym membership, no equipment, and very little time: just a wall and a bit of determination.

As always, if you have hypertension or another cardiovascular condition, it’s a good idea to discuss any major changes to your exercise routine with your healthcare professional before getting started.

The mission of Eureka! is to bring science into everyday life.

If someone in your family or circle of friends has high blood pressure, share today’s article with them. You might help them discover a simple habit that could make a meaningful difference.

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See you tomorrow for another dose of science! 🔬

If you enjoyed today’s article, you might also like our recent evidence-based guide below:

Today is a great day to celebrate science... but perhaps a slightly worse one if you’re dealing with a mouth ulcer. If that’s you, we’re sorry 🙁 you have our sympathy!

Few things are as annoying as a mouth ulcer. That tiny sore seems to appear out of nowhere, and suddenly even drinking water can sting. Then you decide to eat some pineapple... and somehow it gets even worse. Burning, irritation, and sometimes it even feels like new ulcers have appeared.

So what’s actually going on?

Mouth ulcers, also known as aphthous ulcers or canker sores, are small ulcers that develop on the lining of the mouth. They can appear for several reasons, including minor injuries, stress, and changes in immune function.

And maybe it’s just us... but every time we get sick, a mouth ulcer seems to show up too.

That’s not just your imagination. When your immune system is under stress, your body’s ability to maintain the protective lining of your mouth decreases. Tiny injuries that would normally heal unnoticed can develop into painful ulcers.

But what does pineapple have to do with any of this?

Sorry about the AI-generated image, Scientists... the pineapple will only stop looking like this once you subscribe to Eureka!EN and share our newsletter.

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The first culprit is a fascinating microscopic structure called a raphide. Raphides are tiny needle-shaped crystals made of calcium oxalate. Under a microscope they’re beautiful. Inside your mouth... not so much.

Raphides—needle-like calcium oxalate crystals naturally found in pineapple. (Image source: Wikipedia.)

When you bite into fresh pineapple, these microscopic needles can lightly penetrate the lining of your mouth, causing tiny areas of irritation. They’re actually part of the pineapple’s natural defense system against animals.

Yes... the pineapple is literally defending itself from you with microscopic needles 😅

But that’s only half of the story.

Pineapple also contains bromelain, a mixture of protein-digesting enzymes (proteases). That means when bromelain comes into contact with the tissues inside your mouth, it begins breaking down proteins on the surface of your oral mucosa.

Three-dimensional structure of bromelain.

There’s more:

Bromelain can also break down some of the protective mucus in your saliva. Once that protective barrier becomes thinner, the natural acidity of pineapple can irritate the tissue even further.

So you end up with a perfect storm:

• Microscopic raphides create tiny mechanical injuries.

• Bromelain digests proteins in the surface tissue.

• The fruit’s natural acidity further irritates the already vulnerable area.

Together, these factors help explain why pineapple sometimes feels like it’s attacking your mouth, especially if your immune system is already under stress or you already have a mouth ulcer.

The science also explains two surprisingly useful facts.

Have you ever tried making gelatin with fresh pineapple and watched it refuse to set?

Now you know why.

Gelatin is made from collagen, a protein, and bromelain simply cuts those proteins apart before they can form the firm gel structure. Heating the pineapple first destroys bromelain, allowing the gelatin to set normally.

The very same property is also why pineapple is often used as a natural meat tenderizer. Bromelain breaks down muscle proteins, making meat softer.

Science is hiding in the kitchen, too!!

So, what can you do in everyday life?

If pineapple tends to irritate your mouth or make existing ulcers worse, it’s worth avoiding highly acidic foods whenever your mouth is already sensitive or you’re feeling unwell. That includes pineapple, oranges, lemons, strawberries, tomatoes, vinegar, and even soft drinks.

Eating pineapple together with other foods may reduce direct contact between the fruit and your oral tissues. Riper pineapple is usually less acidic and tends to be gentler. Rinsing your mouth with water afterward may also help remove some of the bromelain and reduce the fruit’s acidity, shortening the amount of time these irritating compounds remain in contact with your mouth.

The main inspiration for today’s article was an excellent science communication piece published by McGill University, which includes several additional fascinating facts about pineapple if you’d like to learn more.

If you enjoyed discovering how a simple fruit can teach us so much science, subscribe to Eureka! We bring you evidence-based science every single day.

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Our mission is to make science something people genuinely enjoy learning—but we can’t do it without your help.

So share today’s newsletter, especially with that friend who absolutely loves pineapple.

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Today’s study is a fascinating one. If you’re single, you might get a little worried... just maybe. 😅

Could being married actually lower your risk of developing cancer?

Let’s take a look at the science.

A recent study published in Cancer Research Communications asked exactly that question: does marriage “protect” against cancer?

The researchers analyzed more than 4.2 million cancer cases in adults over the age of 30 using population-based cancer registries from the United States. Here’s what they found:

Among men, cancer incidence was approximately 68% higher. Among women, it was approximately 85% higher. This pattern wasn’t limited to a single type of cancer, it was observed across most major cancer types, different age groups, and multiple racial and ethnic populations.

But let’s slow down, because the story gets even more interesting when we look at the details.

The largest differences were seen in cancers associated with infections and behavioral risk factors.

One of the clearest examples involved cancers linked to human papillomavirus (HPV), a virus primarily transmitted through sexual contact that is associated with several types of cancer.

For example:

• The incidence of anal cancer in men was nearly five times higher among those who had never married.

• Cervical cancer occurred approximately 2.6 times more often among women who had never married.

Transmission electron microscope image of human papillomavirus (HPV). (Image source: Wikipedia.)

A quick public health reminder

Speaking of HPV...

Back to the study...

By contrast, cancers such as breast, thyroid, and prostate cancer showed much smaller differences between married and never-married individuals.

This suggests something important: The apparent “marriage effect” is probably not biological. Instead, it likely reflects differences in health behaviors, lifestyle, and access to healthcare.

The authors note that, on average, married individuals are more likely to smoke less, drink less alcohol, participate in routine preventive screenings, receive greater social support when facing health problems and they may also experience greater financial and emotional stability over the course of life.

But here’s the most important point:

This study does NOT show that getting married directly prevents cancer.

Marital status may simply serve as a marker for other social and behavioral factors that influence cancer risk.

It’s also important to remember that this was an observational study, meaning it can identify associations but cannot establish cause and effect. In addition, the study was conducted in the United States, so the findings may not fully apply to other countries with different healthcare systems, cultures, and social structures.

So what can you actually do with this information?

• Get married...

Just kidding! 😄

The truth is that regardless of your relationship status, the best ways to reduce your cancer risk are the evidence-based recommendations promoted by major cancer organizations.

At Eureka!, we’ve already covered seven modifiable lifestyle factors that can help reduce cancer risk. See below:

Share this article with your single friend! 😉

At Eureka!, our mission is to make science as popular as sports.

If you enjoyed starting your day with science, please share this article!! It really helps us bring evidence-based science to more people.

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Have you ever felt tired in the middle of the afternoon, experienced an unexpected muscle cramp, or noticed that your sleep wasn’t quite as good as usual?

These symptoms can have many different causes, but one nutrient may sometimes play a role: magnesium.

Let’s dive in!

Recent insights published by Harvard Health describe magnesium as the body’s “silent conductor,” participating in more than 300 biochemical reactions.

Rather than acting as a single-purpose mineral, magnesium helps keep countless physiological processes running smoothly. Among its many roles, magnesium contributes to:

• ❤️ Heart function: helps regulate heart rhythm and vascular tone.

• 💪 Muscle and nerve function: supports normal muscle contraction and relaxation, and helps regulate nerve signaling.

• 🦴 Bone health: plays an important role in calcium metabolism.

• 🩸 Metabolic health: adequate magnesium intake has been associated with a lower risk of type 2 diabetes.

• 🧠 Sleep and neurological function: magnesium may influence sleep quality and brain function, although more high-quality research is still needed.

Are You Getting Enough Magnesium?

For most healthy people, magnesium deficiency is uncommon.

The recommended daily intake is approximately:

• 320 mg/day for adult women

• 420 mg/day for adult men

For most people, these amounts are easily achieved through a balanced diet.

Where Can You Find Magnesium?

One challenge of modern diets is the increasing consumption of ultra-processed foods, which tend to contain much less magnesium than whole foods.

Fortunately, magnesium is abundant in many nutritious foods.

A simple rule of thumb:

Excellent dietary sources include:

1. 🌰 Seeds and nuts — Pumpkin seeds are among the richest natural sources.

2. 🥬 Leafy green vegetables — Spinach, Swiss chard, and kale.

3. 🌾 Whole grains — Oats, quinoa, and brown rice.

4. 🍫 Dark chocolate — Yes! High-cocoa dark chocolate (in moderation) also provides a meaningful amount of magnesium.

Examples of magnesium-rich foods.

It’s also worth remembering that the Mediterranean diet naturally provides plenty of magnesium because it emphasizes vegetables, legumes, nuts, seeds, and whole grains. It’s yet another reason why this dietary pattern continues to be associated with numerous health benefits.

So... Should Everyone Take Magnesium Supplements?

Here’s where Harvard Health urges caution:

Unlike magnesium obtained through food—which the body regulates efficiently—magnesium from supplements can accumulate in excessive amounts.

Potential side effects include:

• Diarrhea

• Nausea

• Abdominal cramping

At very high doses, magnesium toxicity may occur, potentially causing:

• Low blood pressure

• Vomiting

• Difficulty breathing

• Cardiac arrhythmias

• Cardiac arrest

Fatal cases of severe hypermagnesemia have been reported, although they are rare.

High-dose magnesium supplements may also interact with certain medications, including antibiotics and some blood pressure medications.

Who May Benefit From Magnesium Supplementation?

Some people are more likely to have low magnesium levels and, in these cases, may benefit from magnesium supplementation. This includes individuals with intestinal disorders, such as Crohn’s disease or celiac disease, since their bodies may have difficulty absorbing this mineral. People with type 2 diabetes may also lose more magnesium through their urine, increasing their risk of deficiency over time.

Other groups include people who consume excessive amounts of alcohol, as this can affect both nutrient intake and nutrient absorption, as well as older adults, who tend to consume less magnesium, absorb less of it through the intestines, and lose more through the kidneys. In addition, the use of certain medications and the presence of chronic diseases may also contribute to lower magnesium levels, which, in some cases, may justify supplementation under medical supervision.

As always, magnesium supplementation should only be used under the guidance of a healthcare professional.

So... Do You Need Magnesium Supplements?

For most people, the answer is probably not.

Magnesium is essential for normal body function, but most healthy adults can obtain adequate amounts through a balanced diet.

Unless you have:

• a confirmed magnesium deficiency,

• one of the medical conditions mentioned above,

• or another specific indication identified by your healthcare provider,

routine supplementation is unlikely to provide additional benefit.

Importantly, the scientific evidence supporting magnesium supplementation remains inconsistent for many health outcomes, and more well-designed clinical trials are still needed.

We’ll definitely revisit this topic as new evidence emerges.

Take-Home Message

🥗 Prioritize a healthy, balanced diet rich in whole foods.

💊 If you suspect you may have magnesium deficiency, talk to your healthcare provider before starting supplements.

⚠️ Don’t assume you need magnesium simply because it’s trending online—marketing often moves faster than the science.

Do you take magnesium supplements? We’d love to hear from you!

📩 Subscribe to Eureka! for free and receive one evidence-based science story every day.

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If you found today’s article useful, share it with someone who may be wondering whether magnesium supplements are really necessary.

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See you tomorrow, scientists! ☕🧬

Science is often described as a solid building, constructed brick by brick through rigorous methods and independent replication.

But what happens when the very first bricks turn out to be fiction?

Today’s Eureka! explores two of the most infamous cases of scientific fraud—one in molecular biology and another in materials physics. Together, they remind us that even the world’s most prestigious laboratories are not immune to deception.

Now that you’re here... let’s dive in!

The “Holy Grail” That Never Existed

Cover of the book referenced in today’s article.

In the early 2000s, the physics community was electrified!

Jan Hendrik Schön, a young researcher at the legendary Bell Labs, appeared to have unlocked the future of electronics by developing organic transistors that promised to replace silicon and revolutionize computing.

As described by journalist Eugenie Samuel Reich in her book Plastic Fantastic, Schön seemed unstoppable!

His work appeared in Nature and Science almost every month, making him one of the brightest rising stars in modern physics.

So... what went wrong?

The data looked too perfect.

An investigation eventually revealed that Schön wasn’t merely adjusting experimental results. He had fabricated entire datasets, creating graphs from scratch using simple spreadsheet functions. The young scientist once considered a future Nobel Prize candidate became the central figure in one of the largest fraud scandals in modern physics.

Sixteen Years Down the Wrong Path in Alzheimer’s Research

A remarkably similar story unfolded in medicine—with even greater human consequences…

In 2006, neuroscientist Sylvain Lesné published a study suggesting that a protein called Aβ*56 was a primary cause of cognitive decline in Alzheimer’s disease. For the next 16 years, this work heavily influenced Alzheimer’s research, directing billions of dollars toward therapies targeting this proposed mechanism.

Alzheimer’s disease is a progressive neurodegenerative disorder characterized by the accumulation of toxic proteins in the brain, leading to neuronal death, memory loss, cognitive decline, and behavioral changes.

Then, in 2022, an investigation by Science, led by neuroscientist Matthew Schrag, uncovered evidence that key images supporting the existence of this specific protein had likely been manipulated through digital image editing.

While researchers around the world pursued treatments based on these findings, enormous amounts of time, funding, and scientific effort may have been invested in a hypothesis built on manipulated evidence.

What Do These Cases Teach Us About Science?

The stories of Schön and Lesné highlight problems that extend far beyond individual misconduct.

1. The Limits of Peer Review

How did rigorous peer review fail to detect manipulations that later seemed so obvious? The scientific publishing system often rewards exciting, groundbreaking discoveries, sometimes at the expense of healthy skepticism.

2. The Pressure to Publish

In highly competitive academic environments, researchers often face intense pressure to “publish or perish.” Science, which ideally progresses carefully and methodically, can become driven by incentives that reward speed, novelty, and high-impact publications.

3. The Cost of Failed Replication

Science is ultimately self-correcting, but correction can be extraordinarily expensive. In physics, laboratories around the world spent years unsuccessfully trying to reproduce Schön’s “breakthroughs.” In Alzheimer’s research, generations of patients waited for treatments that may have been pursuing the wrong biological target.

Science Is a Human Endeavor

These stories should not reduce our confidence in science.

Instead, they remind us that science is a profoundly human activity, shaped by ambition, competition, and occasionally, misconduct.

Whether we’re talking about Schön’s organic electronics or Lesné’s Alzheimer’s research, the lesson is the same:

Transparency, open data, and independent replication are not bureaucratic obstacles. They are the safeguards that prevent the next “scientific breakthrough” from becoming nothing more than another convincing spreadsheet.

Today’s Eureka! was a little different...

Today was all about high-quality scientific gossip. 🍵🔬 Because understanding how science fails is just as important as celebrating when it succeeds.

That’s what makes us better critical thinkers—and less likely to accept the next “miracle discovery” without asking the right questions.

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