Credits: Canva and finnwolfhardofficial/Instagram
The upside-down may be terrifying, but for Stranger Things star Finn Wolfhard, real-life monsters come in the form of panic attacks, spiralling thoughts, and the constant fear of messing up. At just 22, the Canadian actor is choosing not to hide his struggles but instead to shine a light on them, admitting that therapy has become his lifeline.
Wolfhard recently shared in an interview with Variety that his anxiety diagnosis pushed him towards therapy—a decision he calls life-changing. Instead of burying his feelings under back-to-back projects, he has begun facing them head-on. He said that it is something that works for him, adding that therapy has helped him question and confront his fears rather than let them quietly pile up.
Anxiety often manifests as a loop of “what-ifs”, and Wolfhard knows this well. He admitted to frequently worrying about saying or doing the wrong thing, whether in his career, in social settings, or even with fans. This constant self-questioning, familiar to anyone who has battled anxiety, was a big motivator for him to seek professional help.
According to reports, back in 2023, while filming Stranger Things, he regularly experienced panic attacks. On the outside, he looked like a teenager living the dream: global fame, adoring fans, and a blockbuster show. But behind the scenes, he was battling an inner storm. “Everyone thought I was fine,” he recalled. “But really, my brain was changing, anxieties were forming, and I did not know how to process them.” Like many young actors, he learnt to bury these feelings to keep up appearances on set.
Wolfhard’s openness reminds us that therapy is not only for those at breaking point. Often, it is a tool for maintenance, like taking your mind for a regular tune-up. By sharing that therapy has worked for him, he normalises it for his fans, many of whom are in the same age group navigating the pressures of early adulthood. Anxiety can often feel like an invisible weight, and seeking help should be as unremarkable as going to the dentist.
Wolfhard is not alone. Child and teen actors often find themselves under enormous scrutiny before they are emotionally equipped to handle it. Studies show that the entertainment industry’s high-pressure environment, combined with the instability of fame, makes performers particularly vulnerable to mental health challenges. His decision to speak up could encourage others to do the same, breaking the stigma that therapy is something to hide.
By talking about his anxiety diagnosis, panic attacks, and therapy journey, he is showing that even those who seem to “have it all” can struggle too. And maybe the real lesson is that the monsters inside us do not vanish on their own. Sometimes, the bravest thing you can do is not suffering but sitting across from a therapist and saying, “I need help.”
Credits: Health and me
When the COVID-19 pandemic swept the globe, many people instinctively turned to the 2011 film Contagion. What once felt like science fiction suddenly looked disturbingly familiar. The film’s accuracy in depicting how viruses travel—through handshakes, doorknobs, and elevator buttons—was a chilling reminder of how quickly infections can move in a connected world.
One line from Kate Winslet’s character stood out, every pathogen carries a number, R0 (R-nought), that tells us how many people, on average, one infected person will pass the disease to. A value above one means a disease can spread. A value below one suggests it will fizzle out over time.
That deceptively simple number, however, hides enormous complexity. Different diseases spread in very different ways: through coughing, sneezing, contaminated food, or even insect bites. And while some infections burn through populations at lightning speed, others move more slowly but cause devastating damage. Understanding the contagion scale isn’t just academic—it shapes how we protect ourselves, our families, and our communities.
R0 is not a fixed property of a pathogen—it reflects biology, behavior, and environment. Think of it as the interaction between how contagious the germ is, how people interact, and what protections are in place.
For example, a crowded subway system in winter gives respiratory viruses a much higher chance of spreading than the same virus in a rural outdoor community. Vaccination rates, cultural norms around close contact, and even building ventilation play a role.
Still, the R0 scale gives us a useful way to rank which diseases have the highest potential to spread—and which, while less contagious, still carry grave risks.
No disease outpaces measles when it comes to raw transmissibility. With an R0 between 12 and 18, it sits at the very top of the contagion scale. To put that in perspective: one person with measles could, after just two rounds of transmission, set off a chain reaction infecting more than 300 people.
Part of measles’ power lies in how it spreads. The virus is airborne, carried in microscopic droplets that linger in the air for hours. You don’t even need to meet the infected person—walking into a room they left behind is enough for an unvaccinated individual to catch it. Worse, people with measles are infectious before they show symptoms, meaning isolation often comes too late.
Despite being preventable, measles has resurged in recent years, even in wealthy nations. Falling vaccination rates—driven by pandemic disruptions, conflict, and persistent vaccine misinformation—have left gaps in herd immunity. Beyond its immediate fever and rash, measles can cause pneumonia, seizures, blindness, and in rare cases, death.
Measles may lead the pack, but it isn’t alone in its ability to spread rapidly.
With an R0 of 12 to 17, pertussis primarily affects children but can be transmitted by adults with milder symptoms. Severe coughing fits can lead to broken ribs, pneumonia, or even death in infants.
Often dismissed as a childhood rite of passage, chickenpox has an R0 of 10 to 12. Though usually mild, it can cause serious complications such as encephalitis or bacterial infections, especially in adults.
Depending on the variant, COVID’s R0 has ranged from 2.5 in early strains to as high as 12 in Omicron subvariants. Its spread underscored how a “moderately contagious” pathogen can cripple global systems when paired with global travel and asymptomatic transmission.
While these diseases differ in severity, their shared trait is efficiency of spread. Each one demonstrates how quickly a community can be destabilized when vaccination or preventive strategies falter.
Not all deadly diseases spread like wildfire. Some move more slowly but pose equally serious threats.
Tuberculosis (TB), caused by Mycobacterium tuberculosis, has an R0 ranging from less than one to four. That lower figure reflects the fact that TB usually requires long, close exposure—often in households, shelters, or prisons. But the slower spread belies the challenge: TB is extremely difficult to treat, requiring at least six months of multi-drug therapy. Cases of drug-resistant TB are rising, threatening to undo decades of progress.
Ebola, another disease with frightening lethality, has an R0 of just 1.5 to 2.5. It spreads only through direct contact with bodily fluids, which helps explain why outbreaks, while devastating, tend to remain geographically contained. Still, Ebola kills up to 90% of those it infects, making containment absolutely vital.
Diseases such as MERS, avian flu, and leprosy have R0 values below one, meaning they are unlikely to cause sustained outbreaks under current conditions. Yet their low spread does not equal low risk—when these pathogens do infect, they can cause severe complications or death.
Understanding modes of transmission is as important as R0 values. Respiratory droplets and aerosols drive infections like flu, COVID, and measles. Blood-borne and vector-borne diseases (HIV, malaria, Zika) move through different pathways—sexual contact, shared needles, or insect bites. Food- and water-borne illnesses such as cholera or hepatitis A highlight how sanitation and clean water infrastructure remain frontline defenses.
Every route of transmission offers a point of intervention. Handwashing, clean water, mosquito control, safe sex practices, and above all, vaccination programs are proven to reduce spread.
No discussion of infectious spread is complete without herd immunity. When enough people in a population are immune either through vaccination or prior infection, the chain of transmission is broken. This protects not only the individual but also those who cannot be vaccinated, including infants, pregnant women, and people with compromised immune systems.
The resurgence of measles and pertussis is not due to new strains or failures of medicine it’s due to falling herd immunity. The collective shield works only if most people contribute.
The contagion scale reminds us that “contagious” is not the same as “dangerous.” A disease can spread quickly and cause little long-term harm, or spread slowly but devastate those it touches. Both demand vigilance.
What COVID-19 demonstrated, and what measles continues to prove, is that human behavior—whether it’s embracing vaccination, staying home when sick, or even improving ventilation in schools and workplaces—shapes the trajectory of outbreaks as much as the biology of the pathogen itself.
(Credit-Canva)
A sixth person has died from the Legionnaires’ disease outbreak in Central Harlem, according to New York City health officials. The city is currently investigating the outbreak that began in late July, which has now affected over 100 people.
As of Thursday, 111 people have been diagnosed with the disease. The recent death was of a person who passed away outside of New York City earlier this month, but their death was only recently linked to the outbreak. There are currently seven people hospitalized.
The city has identified and cleaned 12 cooling towers on 10 buildings, including a city hospital and a clinic, where the bacteria were found. These cooling towers, which use water to cool buildings, are believed to be the source of the outbreak.
Legionnaires' disease is a severe type of pneumonia caused by a bacteria called Legionella. This bacteria thrives in warm water and can spread through a building’s water system. People usually show flu-like symptoms, such as a cough, fever, and muscle aches, within two days to two weeks after they are exposed to the bacteria.
Health officials are advising anyone who lives or works in the Central Harlem area to contact a doctor if they experience these symptoms.
The disease often starts like a mild flu. For the first couple of days, you might have muscle aches, body aches, and headaches. But after this initial phase, the symptoms get much worse.
You might develop a high fever of 100.4°F or higher, along with chills and extreme tiredness. About half of the people who get sick also experience confusion or delirium. Other symptoms include an upset stomach, with nausea, vomiting, and diarrhea. Since the bacteria attack the lungs, you will likely have a persistent cough that can start out dry but may later produce mucus or even blood. You may also feel short of breath and have chest pain.
The time it takes for you to get sick after being exposed to the Legionella bacteria is called the incubation period. It can be as short as two days or as long as 19 days. Most people, however, start feeling sick around six to seven days after they've been exposed. This is the time the bacteria need to grow inside your body before they cause noticeable symptoms.
Pontiac fever is a milder version of the same infection. Its incubation period is much shorter, usually just one to two days. The symptoms are less severe and include a flu-like sickness with muscle pain, headaches, and a fever. Unlike Legionnaires' disease, Pontiac fever usually goes away on its own without needing a lot of medical care. Because it is so mild, doctors sometimes don't even realize it's Pontiac fever.
Doctors can figure out if you have Legionnaires’ disease using a few different tests. They will often check your blood and urine or look for the bacteria in a sample of your sputum (the mucus you cough up). They may also take a chest X-ray, but this can be tricky because the results look like other types of pneumonia.
The best way to get a clear diagnosis is through lab tests that can directly identify the bacteria. It's also a clue that you have it if your illness doesn't get better with common antibiotics like penicillin. Without treatment, the illness can get much worse and may lead to serious problems like kidney failure, respiratory failure, and even death.
Credits: iStock
Stem cell transplantation has long stood as one of medicine’s most powerful tools, offering hope to patients with genetic disorders, immune deficiencies, and blood cancers. But it comes at a staggering cost: before healthy donor cells can take root, patients typically undergo toxic chemotherapy or radiation to destroy their own diseased bone marrow. The side effects can be devastating — infertility, organ damage, secondary cancers, and sometimes death.
Now, researchers at Stanford Medicine have shown it doesn’t always have to be this way. A Phase 1 clinical trial published in Nature Medicine has demonstrated that an antibody-based treatment can safely prepare patients for a stem cell transplant without using busulfan chemotherapy or radiation. For children with Fanconi anemia, a rare genetic disorder that makes conventional transplants particularly dangerous, this represents nothing short of a medical breakthrough.
Traditionally, transplants hinge on “conditioning” — a process to clear out faulty bone marrow so donor cells can settle in. Until now, that has required high doses of chemotherapy or radiation, treatments that damage DNA and leave lifelong scars.
The Stanford team instead used briquilimab, an antibody that targets CD117, a protein on blood-forming stem cells. By binding to CD117, the antibody wipes out diseased stem cells without blasting the rest of the body with toxins.
“We were able to treat these really fragile patients with a new, innovative regimen that allowed us to reduce the toxicity of the stem cell transplant protocol,” said Dr. Agnieszka Czechowicz, MD, PhD, assistant professor of pediatrics and co-senior author of the study.
For Fanconi anemia patients, who are hypersensitive to DNA damage, eliminating busulfan and radiation could be life-saving.
The Phase 1 trial enrolled three children with Fanconi anemia, each younger than 10 years old. Instead of the usual conditioning, they received a single infusion of briquilimab 12 days before transplant, followed by low-intensity immune suppression but no chemotherapy or radiation.
The donor bone marrow came from their parents — genetically half-matched but specially prepared. Researchers enriched it with CD34+ stem cells while removing alpha/beta T-cells, immune cells known to trigger graft-versus-host disease.
The results stunned the team. Within two weeks, the donor stem cells had taken hold. By 30 days, healthy blood production was underway. Two years later, all three children have nearly 100% donor cells in their bone marrow, far exceeding the trial’s goal of just 1%.
“No one experienced graft rejection, and the outcomes were better than we had dared to expect,” Czechowicz said.
This success is decades in the making. Stanford’s Dr. Irving Weissman first studied CD117 antibodies in mice nearly 20 years ago. Step by step, researchers refined the science until a clinical-grade antibody was ready for human trials.
The first child to benefit was 11-year-old Ryder Baker from Texas. Before his transplant, Ryder was exhausted by his illness. “He was so tired, he didn’t have stamina,” recalled his mother, Andrea Reiley. Today, Ryder is thriving — playing soccer, enjoying pickleball, and even earning the title of “Up and Coming Player” at school.
Reiley says her son takes pride in being a pioneer. “I have conversations with him about how his experience is helping doctors take better care of other kids. I think he takes a lot of pride in that too.”
Fanconi anemia is a genetic disorder of DNA repair. The body’s stem cells can’t fix everyday DNA damage, leading to progressive bone marrow failure. Children often develop fatigue, infections, and bruising before age 12. Without a transplant, they face life-threatening complications.
But because their DNA-repair machinery is so faulty, standard chemo or radiation is especially harmful. “Right now, nearly all of these patients get secondary cancers by the time they’re 40,” Czechowicz noted.
The antibody-based method offers a way out of this deadly paradox, a path to transplant without the genotoxic conditioning that accelerates cancer.
Another innovation lies in how donor cells are prepared. For decades, 35–40% of patients never received transplants simply because they lacked a perfectly matched donor. Using half-matched donors like parents — while carefully engineering the graft to reduce complications — expands the donor pool dramatically.
“We are expanding the donors for stem cell transplantation in a major way, so every patient who needs a transplant can get one,” explained Dr. Rajni Agarwal, MD, co-first author and professor of pediatric stem cell transplantation.
This has profound implications not only for Fanconi anemia, but also for other inherited blood disorders like Diamond-Blackfan anemia and even some immune deficiencies.
Stem cell transplants are most commonly used in blood cancers like leukemia and lymphoma. While cancer patients may still require some chemotherapy or radiation to clear malignant cells, researchers believe antibody-based conditioning could benefit those too frail for full-dose regimens — including elderly patients.
Another Stanford team is already exploring whether briquilimab could be used in this vulnerable population.
“We may finally have a way to treat these patients with less intensity, so it’s possible for them to get a transplant,” Agarwal said.
Even with this breakthrough, transplants remain grueling. Ryder and the other children spent over a month in the hospital, battling side effects like exhaustion, nausea, and hair loss. And there is the broader issue of drug availability. Briquilimab is still in clinical trials, and scaling up access will take time.
Still, for families who once faced impossible odds, the difference is profound. “When I counsel families, their eyes start to shine as they think, ‘OK, we can avoid the radiation and chemo toxicity’,” Agarwal said.
The Stanford team is now running a Phase 2 trial in more children with Fanconi anemia, and they plan to extend the approach to other disorders. Longer-term, researchers hope antibody-based regimens can be combined with gene editing therapies — replacing faulty genes while avoiding the toxic prep work.
Czechowicz believes this is just the beginning, “We were optimistic, but we’ve been surprised by how well it’s worked. This could redefine how we think about stem cell transplantation.”
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