Fresh Air Saved Lives in 1918. We Sealed COVID In.
In 1918, doctors did something obvious.
They opened the windows.
They dragged beds outside. Set up tents. Let people breathe.
That’s what saved lives during the deadliest pandemic in modern history. It wasn’t complicated technology. It wasn’t miracle drugs. It was air.
Simple, free, moving air.
Then we sealed ourselves in.
By 2020, we had a century of science telling us exactly how respiratory viruses spread. We knew the patterns. We had the research. We had better tools, better technology, better everything.
And we still got it wrong.
We told people to lock down inside.
We sealed our windows shut.
We blocked access to beaches and parks.
Then acted bewildered when infection rates soared.
How Nature Healed in 1918
The evidence was crystal clear a century ago. You get infected quicker indoors. You recover slower indoors.
Indoors is where disease thrives.
Doctors in 1918 weren’t fighting misinformation campaigns or pharmaceutical influence. They were watching sailors die and trying what worked.
At Camp Brooks Hospital in Boston, they rolled the sickest patients outside—men who’d been crammed in the stale, airless quarters of naval ships. Death rates plunged from 40 percent to 13 percent. Just changing where people breathed cut mortality by two-thirds.
This wasn’t experimental. It was protocol.
The Massachusetts Surgeon General declared open-air treatment “absolutely proven.” Not recommended. Proven.
Doctors flung open every hospital window. Treated patients in direct sunlight. Let air flow continuously.
And people survived.
Archives show it clearly. Black-and-white photographs of soldiers lying in rows under open sky, bundled in blankets. Nurses in heavy coats providing care without high-tech filters or negative pressure rooms. Just air. Natural air.
It saved lives.
School Without Walls
When the 1918 pandemic threatened schools, officials didn’t waste months fighting about masks or pretending kids couldn’t spread disease.
They didn’t trap children between education and safety.
They moved class outside.
The open-air school movement had begun years earlier to combat tuberculosis. When influenza arrived, they already had the blueprint.
Children learned on ferry decks. On rooftops. In parks. They wore extra layers. They kept gloves on. They continued learning—in clean, flowing air.
No remote learning technology. No HEPA filters. Just fundamental public health logic: studying in cold, circulating air beats sitting in warm, stagnant air.
In 2020, we pretended our only options were unsafe indoor classrooms or isolated screen time. We ignored our own history.
We could have adapted. We could have solved this.
Instead, we argued and divided.
Architecture That Protected Us
We didn’t just understand ventilation. We built for it. Post-1918, architects internalized the lesson: trapped air kills.
So they designed solutions. Radiators were deliberately oversized to heat rooms even with windows wide open. That wasn’t accidental.
When your apartment overheats in January, that’s not poor design. That’s intentional protection.
Your radiator is doing exactly what it was built to do—keep you warm enough to let fresh air in during a pandemic.
These heating systems weren’t about luxury. They were survival mechanisms for open-window living. For air circulation, not air trapping.
Then came the energy crisis. Weather stripping. HVAC systems. We sealed our buildings tight. We prioritized efficiency over health.
When COVID-19 hit, we acted like airflow was some radical new concept.
2020 to Now, Ignoring What Works
We had supercomputers. Advanced engineering. Environmental sensors.
We had 100 years of medical literature.
And we still behaved like COVID spread through dark magic.
We sanitized groceries obsessively.
We fought over toilet paper.
We installed flimsy plastic dividers that trapped viral particles like terrariums.
The one basic thing we refused to do?
Open our goddamn windows.
Ventilation was dismissed as unscientific. Outdoor activities were regulated into oblivion.
Meanwhile, classrooms and workplaces turned into virus incubators. No air exchange. No fresh breezes. Just recycled breath.
We told children to eat silently in classrooms with thirty other kids and a single box fan.
We told employees to return to offices with sealed windows and inadequate ventilation.
We normalized danger.
Not because we lacked information.
Because we refused to face reality.
Buildings That Suffocate
Modern construction creates perfect virus chambers.
Sealed to trap heat, block sound, and prevent air movement.
We value energy ratings over human health.
When COVID—a pathogen that floats through air like cigarette smoke—arrived, we locked ourselves inside the perfect delivery system.
Look at where major outbreaks clustered:
Schools.
Care facilities.
Meat plants.
Correctional facilities.
Places where windows don’t open and ventilation is afterthought.
These are our architectural ideals.
Airtight boxes. Recirculated air.
Climate-controlled petri dishes.
Change Is Still Possible
Here’s what nobody wants to acknowledge.
We can still fix this.
You can crack your window right now.
You can meet people in parks instead of packed restaurants.
You can put air purifiers in your living spaces.
We don’t need pharmaceutical salvation.
We need to stop poisoning ourselves with our own exhaled breath.
We could redesign classrooms that don’t spread disease.
We could build workplaces that protect human health.
We could require ventilation ratings on every public building entrance like we do food safety scores.
But that would require admitting our mistakes.
That would mean confronting uncomfortable truths.
And our systems aren’t built to profit from prevention.
Open Air Is Self-Defense
In 1918, they had few alternatives.
They were forced to trust nature.
Now, we have choices. And we consistently choose wrong.
Fresh air isn’t some wellness luxury. It’s not decor. It’s not optional.
It’s the most fundamental intervention that works.
The longer we ignore this reality, the longer COVID will haunt us.
Future pandemics too.
We keep fantasizing about returning to normal.
But our normal is what created this disaster.
How to Love Someone With Long Covid (Even When It’s Hard)
Let’s talk about something brutal.
When you get sick and stay sick, people disappear. That’s not a flaw in your personality or your worth. That’s human behavior. Animal behavior, actually.
Let me rewind.
Decades ago, I dated someone I loved deeply. She had this deep belief, that if the passion fizzled, it was over. That was the whole rulebook for her: no fireworks, no future. And maybe when you’re young, that feels like truth. But I had already seen what love actually looks like, the kind where your parents argue. and then hold hands shortly after. The kind where frustration turns into listening, and listening, turns back into love, like some weird emotional tide.
So when she asked me, “Is it over?” I was confused. Like… why would she even think that?
Later, I learned something that changed me.
You don’t have to feel love to show it.
Almost always, the showing comes first.
When you do the loving thing as a caregiver, lover, friend, and cook their favorite meal, run the errand, sit through their bad day, something inside shifts. Love grows out of the act in you. It’s a feedback loop. Not a feeling. A practice. Both of my deepest relationships got stronger the moment I stopped chasing emotional proof and just acted out of little acts of me doing loving things. And you know what? The feeling always followed. I loved them more. I was loved back more.
This is where we bring in Long Covid.
Millions of people have been living through something that most of the world pretends isn’t real. Something that doesn’t show up on the surface, but eats through their body, their energy, their memory, their sense of self. And if they are lucky enough to have a partner, or a parent, or a friend who’s still around, chances are, you are also struggling.
Because illness drives people away.
It always has.
It’s not new. Throughout history, when people got sick, they got abandoned. Leprosy. Tuberculosis. Polio. People didn’t just suffer the disease, they suffered being cast out.
We’re no different. Just more polite about it.
And if you’re the one still here, caring for someone who’s chronically ill, let me say this: Your instincts will betray you. There’s a weird effect that illness has on caregivers. It makes you want to retreat. You’ll find yourself pulling away. Not because you’re cruel. But because your brain is screaming for safety. Normalcy. Simplicity. And right now, the sick person you love is the opposite of that.
This is where I remind you: You are an animal.
I listen to this podcast called Tooth and Claw. It’s full of bear attacks and wild animal stories. One of the hosts says something that stuck with me:
“If you see a behavior in animals across a wide population, it’s probably an animal behavior.”
Well guess what? Caregivers disappearing when someone gets sick, and that’s an animal behavior. Human animal behavior. Our biology is hardwired for survival, and that means distancing from perceived danger. Sickness triggers something ancient in us. Something deep. Something hard to override.
But here’s the thing.
You can override it.
It starts with remembering who they are, not who they are now, in bed, groaning, or angry, or falling apart, but who they were. Who you fell in love with. Who made you laugh until you cried. That version of them still exists, even if it’s buried under symptoms and fatigue and grief.
Remember this too: In sickness and in health wasn’t poetic fluff. That vow wasn’t written for fairy tale weddings. It was a survival pact. It came from generations of people who watched their children die of infections. Who lost partners to fevers. Who suffered and stayed. That phrase was carved out of real history, when illness wasn’t rare (Just look up how many children died pre-1930s) it was expected. And now here we are again.
Modern medicine gave us the illusion that we were safe. That sickness was temporary. That suffering was manageable. But Long Covid shattered that illusion. And most people born after 1960 have no emotional blueprint for this.
We’re flying blind.
If you’re the one who’s sick, here’s something you need to hear: You’re not being ignored because you’re annoying or boring or selfish. You’re being ignored because your suffering triggers something ancient and uncomfortable in people. They don’t know how to sit with it. Most weren’t taught how. Their avoidance isn’t always a conscious choice. It’s an emotional reflex.
In the book How Emotions Are Made, Lisa Feldman Barrett explains that emotions come first, and logic comes after. We don’t decide how to feel — we feel, and then decide based on that. So when your loved one shrinks from your pain, or snaps at you, or stops checking in, ask yourself: Are they choosing that? Or is it an emotional response they don’t even recognize?
Think about the last time you stubbed your toe on something, and shouted at an inanimate object. “Damn it!” That wasn’t a planned reaction. That was your animal brain in action.
That’s what we’re dealing with. Not cold indifference. Biology.
So what can you do?
If you’re a caregiver, do one loving thing today. Not because you feel warm and fuzzy. But because it’s the right thing. Make tea. Rub their back. Sit in the room quietly. Do it even if they don’t thank you. Do it even if they’re upset. Because the feedback loop still works. It works on you. You’ll feel more love just from acting in love.
If you’re a patient, and your family member is cold or distant, try this: If you have the energy, think a loving thought toward them. Even if they’re not giving it back. Just thinking it can soften something inside you. Maybe it leaks out. Maybe it doesn’t. But you’ll feel it. And maybe — just maybe — that loop starts to close.
None of us chose this.
But we can choose how we respond.
We’re not just animals.
We’re animals with memory.
With words.
With stories.
I know I tend to make long posts. I’m going to include an audio version for those who can’t read long posts. For future articles, I’m definitely open to suggestions fiture posts. Should they be shorter or should they be broken up with titles?
Is their evidence for viral persistence in COVID-19?
From the meticulous work of the PolyBio Research Foundation, in collaboration with the esteemed halls of UC San Francisco and Harvard Medical School, to the robust findings published in Nature and The Lancet, we are presented with compelling evidence of the virus’s tenacity.
These studies not only confirm the presence of viral proteins and RNA months after the acute phase of infection but also suggest a troubling link to the chronic, debilitating symptoms known as long COVID.
Let’s delve into some of the evidence for the evidence pointing to viral persistence of SARS-CoV-2,
1. PolyBio Research Foundation Study
A study published by the PolyBio Research Foundation, supported by UC San Francisco and Harvard Medical School, found that viral proteins from SARS-CoV-2 could persist in the body for up to 14 months post-infection. This study used an ultra-sensitive blood test to detect viral proteins in 25% of the 171 participants, indicating that the virus can linger in tissues and organs long after recovery from the acute phase of the infection. The likelihood of detecting these proteins was higher among those who were hospitalized or reported severe symptoms during their initial infection[1].
2. Nature Study on Persistent SARS-CoV-2 RNA Shedding
A cohort study published in *Nature* identified persistent SARS-CoV-2 RNA shedding in individuals for at least 30 days, with some cases extending to 60 days. The study found that individuals with persistent infections had more than 50% higher odds of reporting long COVID symptoms compared to those with non-persistent infections. This suggests that persistent infections could contribute to the pathophysiology of long COVID, although the exact mechanisms remain to be fully understood[3].
3. NCBI Study on Long COVID and Viral Persistence
Research published on NCBI proposed a hypothesis-driven model for long COVID, suggesting that the persistence of SARS-CoV-2 or its components (such as the spike protein) could lead to chronic inflammation and a dysregulated immune response. This model is supported by evidence of viral RNA and antigens being detected in various tissues, including the cerebrospinal fluid and feces, months after the initial infection. The study highlights the potential for viral persistence to trigger long-term health issues[2].
4. Lancet Study on Viral Persistence in Tissues
A study published in *The Lancet* examined the persistence of SARS-CoV-2 in various tissues, including blood, gastrointestinal, and surgical samples. The research found that viral RNA and proteins could be detected in these tissues long after the acute phase of infection, suggesting that the virus can persist in different parts of the body and potentially contribute to ongoing symptoms and health complications[5].
5. NCBI Study on Viral Persistence and Reactivation
Another study on NCBI explored the persistence of viral RNA and antigens in patients with long COVID. It found that viral components could be detected in blood, stool, and urine, and that the presence of these components was associated with persistent symptoms. The study also noted that viral persistence might involve either active replication or the presence of non-replicating viral RNA, which could still trigger immune responses and inflammation[4].
The evidence from these studies collectively supports the notion that SARS-CoV-2 can persist in the body for extended periods, potentially leading to long-term health issues such as long COVID. This persistence can involve both active viral replication and the presence of viral components that continue to stimulate the immune system, leading to chronic inflammation and other symptoms.
Further research should be done to put to rest this question of viral persistence and to develop effective treatments for long-term COVID.
A study reveals that SARS-CoV-2 can infect human CD4+ T helper cells, impacting the immune response in severe COVID-19 cases. The virus uses the CD4 molecule to enter these cells, leading to functional impairment and cell death. This infection results in increased IL-10 production in T cells, associated with viral persistence and severe disease. The findings suggest that SARS-CoV-2 infection of CD4+ T cells contributes to immune dysfunction in COVID-19.