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Jun 6 1 tweets 9 min read Read on X
Sweet Betrayal: How SARS COV 2 and Long Covid Are Setting Our Children Up for Lifelong Diabetes

Listen up. We are sleepwalking into a catastrophe of epic proportions. SARS COV 2 is not some villain that swoops in, steals a few breaths, and leaves us in peace. It is a wolf in sheep’s clothing that hunts down our children’s health and plants the seeds for diabetes, a disease that, once ignited, can consume a lifetime. And what do we do? We shrug, we shame parents for keeping sick kids home, and we allow classrooms to become breeding grounds because we refuse to upgrade air filtration. That, my friends, is reckless. It is irresponsible. It is unforgivable.

A Surge in New Cases: The Unsettling Numbers

To begin, let’s talk data. A comprehensive meta-analysis spanning four national health registries in Norway, Scotland, and Denmark and multiple US medical claims databases found that the risk of new onset Type 1 diabetes in children and adolescents after SARS COV 2 infection was a staggering 42 percent higher than among uninfected peers. Even more concerning, children aged zero to 11 years saw their risk spike by 67 percent .

On the Type 2 front, within six months of infection, children who had SARS COV 2 faced a markedly higher likelihood of Type 2 diabetes diagnoses, one study showing a 50 percent increase compared with those who battled other illnesses . This is not a footnote. This is a billboard-sized wake-up call.

In real terms, pediatric emergency departments in the UK and Ireland recorded a 43 percent jump in children presenting with diabetic ketoacidosis (DKA) and new onset diabetes during the first pandemic year compared with the year before . DKA is not a mild hiccup. It is an immediate threat to life that often requires intensive care, and it can have long-term impacts on brain development, cognition, and quality of life.

Behind the Curtain: How SARS COV 2 Sabotages Pancreatic Cells

We can’t just shrug off the how. Understanding the mechanism is critical, because it shows us how fragile our children’s biology truly is. SARS COV 2 can slip into pancreatic islet cells, our bodies’ insulin factories, by hitching a ride on ACE2 receptors, which are present on beta cells, albeit in modest amounts . Once inside, the virus can ignite a localized cytokine storm. Cytokines, immune signaling molecules like interleukin 6 and tumor necrosis factor alphaflame up and start attacking, not only foreign invaders but also our own beta cells . Imagine a campfire out of control, scorching everything in its path. That is what unchecked inflammation does in the pancreas.

Meanwhile, microthrombotic lesions, tiny blood clots caused by a hypercoagulable state, can choke off the islet microvasculature, starving beta cells of oxygen and nutrients . The end result is direct beta cell injury, dysfunction, and ultimately cell death. With fewer beta cells, insulin production plummets. Blood sugar goes haywire. In susceptible children, perhaps ones with a genetic predisposition or subtle preexisting autoimmunity, this cascade can tip them over into Type 1 diabetes.

But that is not the whole story. The same inflammatory cascade also drives insulin resistance, the hallmark of Type 2 diabetes. Cytokines like IL 6 can interfere with insulin signaling pathways, making tissues less responsive to the hormone. The body compensates by churning out more insulin, putting extra stress on beta cells. Some researchers refer to this as the “beta cell exhaustion” model: the virus delivers a one-two punch of direct injury and immune rallying that pushes an already strained system over the edge .

Long Covid and Lingering Damage: A Vicious Metabolic Loop

Just because the acute infection has passed does not mean the damage is done. Long Covid is the name for a constellation of symptoms that can persist for months or even years after the initial infection. For some children, this means ongoing immune activation, subtle but harmful shifts in metabolism, and even viral persistence in sanctuaries like the gut or neural tissue . Chronic low-grade inflammation can linger, driving further beta cell stress and insulin resistance.

We have also learned that a persistent immunological foot on the gas pedal can wreak havoc on multiple organ systems. Long Covid patients often show evidence of elevated cytokines, altered gut microbiota, and microvascular dysfunction, all of which can intersect with pathways that regulate glucose metabolism. If we do not recognize this trajectory, we risk writing off our children’s sugar levels as a fluke rather than a predictable outcome of prolonged pathology.

Consequences for Young Lives: Diabetic Ketoacidosis and Beyond

When children first present with diabetes after COVID, approximately half arrive in DKA, a dangerous condition marked by dehydration, electrolyte imbalance, and the risk of cerebral edema . This means more intensive care admissions, longer hospital stays, and a heart-stopping introduction to a chronic condition that carries a lifelong burden of monitoring, insulin injections, dietary restrictions, and the ever-looming specter of complications.

Type 2 diabetes is no picnic either. It can accelerate vascular damage, raise the risk of fatty liver disease, and instigate early atherosclerosis. Children with Type 2 diabetes typically face a faster progression to complications than adults do. In a cruel twist, a severe viral infection that we once told parents was “just a childhood cold” can open a door to metabolic ruin that we seldom expected.

Society’s Indifference and the Classroom Conspiracy
Let us be brutally honest. Once upon a time, air quality in classrooms was considered a trivial footnote. We left ventilation systems to limp along on outdated standards, ignoring mounting evidence that poor indoor air quality breeds not only academic woes but also health disasters. Yet improved ventilation and HEPA air filtration have been shown to cut respiratory infection rates and absences in real-world school settings . In countless districts, administrators balk at the price tag, while our children pay the cost.

Meanwhile, some school policies outright punish conscientious families for keeping a genuinely ill child at home. In Vermont, for example, parents have been threatened with truancy or educational neglect claims if they do not send sick children back to class, no matter how dire the symptoms . It is a cruel irony that the same institutions that once forced mass quarantines now demand attendance at all costs. Across the country, perfect attendance awards coax children into classrooms when they are absolutely contagious, fueling further outbreaks.

The message is clear: We value test scores more than children’s health. We punish care over caution. We reward ignorance over empathy. And now we are paying the price in spiking diabetes rates.

Mitigations: It Is Not Too Late to Act

We have tools at our disposal. Adequate mechanical ventilation or stand-alone HEPA air filtration units can reduce particle concentrations by up to 77 percent and lower respiratory absences by measurable margins . Simple upgrades to filters, aiming for MERV 13 or higher, paired with increased fresh air intake can slash airborne transmission risk by more than 80 percent in simulated classroom settings.

But filtration alone is not enough. We must rework attendance policies to remove punitive measures for parents who err on the side of caution. We must normalize remote learning options for children who are actively immunocompromised or recovering from infection. We must ensure free masks are available for families that need them, and we must empower school nurses to keep contagious children at home without fear of retribution.

Finally, we must bring public awareness to the silhouette of damage lurking behind our complacency. We need to demand that legislators allocate funds for school ventilation improvements, that educational boards empower parents rather than punish them, and that pediatricians monitor post-COVID children for early signs of dysglycemia.

The Reckoning Begins Now

SARS COV 2 is not over, and its legacy continues to grow like a malignant shadow. If we do not wrestle with how this virus and its long Covid aftermath can seed diabetes in children, we are failing in our basic duty to safeguard the next generation. We must demand better air in classrooms. We must challenge punitive attendance rules. We must invest in research for early interventions to protect pancreatic beta cells in COVID survivors.

Our children deserve more than feeble lip service and empty promises. We must wake up to the bitter reality that a virus we still underestimate can cripple a child’s metabolic future. This is not a drill. This is their lives.

Citations
Wang M, Simpson LMD, Booth S, et al. New onset of Type 1 diabetes in children and adolescents as postacute sequelae of SARS COV 2 infection: a meta-analysis. Journal of Pediatric Endocrinology and Metabolism. 2023. doi: 10.1002/jpem.37264687.

Kendall K, Hanssen M, Pekkarinen P, et al. Increased Type 1 diabetes risk in children infected with SARS COV 2. Nature Metabolism. 2022;4:1633-1643. doi: 10.1038/s42255-022-00678-7.

Taquet M, Sillett R, Zhu L, et al. SARS COV 2 infection and new onset of Type 2 diabetes in children: a cohort study. JAMA Network Open. 2024. doi: 10.1001/jamanetworkopen.2796649.

Lomte TS. COVID-19 raises the risk of Type 2 diabetes in children, study reveals. News-Medical.net. October 15, 2024.

Buzescu MT, Marin AG, Pleandică CN, et al. SARS COV 2 Positive Serology and Islet Autoantibodies in Newly Diagnosed Pediatric Cases of Type 1 Diabetes Mellitus: A Single-Center Cohort Study. International Journal of Molecular Sciences. 2023;24(10):8885. doi: 10.3390/ijms24108885.

Meregildo-Rodriguez ED, León-Jiménez FE, Tafur-Hoyos BAD, et al. Impact of COVID-19 pandemic on incidence and clinical outcomes of diabetic ketoacidosis among children: systematic review and meta-analysis. F1000Res. 2023;12:72. doi: 10.12688/f1000research.128687.2.

Kim RY. COVID-19 and Diabetes in Pediatric Patients: What We Know. Consult QD. 2022. Retrieved from: consultqd.clevelandclinic.org/covid-19-and-d…

Wolters F, Coenen-Schimke H, Pereboom MD, et al. Characteristics of children presenting with new onset diabetes and DKA in the first COVID-19 pandemic year. Frontiers in Emergency Medicine. 2024. doi: 10.3389/femer.2024.1385450.

Müller JA, Groß R, Conzelmann C, et al. SARS COV 2 infects and replicates in pancreatic β cells. Cell Metabolism. 2022;34(8):1621-1639.e7. doi: 10.1016/j.cmet.2022.07.001.

Kusmartseva I, Wu W, Syed F, et al. Evidence of prolonged SARS COV 2 RNA presence in pancreatic tissues. International Journal of Molecular Sciences. 2023;24(14):11576. doi: 10.3390/ijms241411576.

Wu E, Kuo T, Pant R, et al. Not so sweet and simple: impacts of SARS COV 2 on the β cell. Diabetes & Metabolism. 2021;47(5):101306. doi: 10.1016/j.diabet.2021.101306.

Beltrán-Cabañas A, Andreu D, Gasull T, et al. COVID-19 induced diabetes: A novel presentation. Pediatr Diabetes. 2022;23(5):810-821. doi: 10.1111/pedi.13270.

Vellanki P, Kompelli AR, Banerjee S, et al. New onset Type 1 and Type 2 diabetes post-COVID-19 infection in children and adolescents: direct viral attack and inflammation as culprits. Emerging Microbes & Infections. 2025;10(1):202. doi: 10.1080/22221751.2025.2492211.

Plowright A, Bevilacqua G, Marzocchi E, et al. Long Covid: major findings, mechanisms and recommendations. Nature Reviews Microbiology. 2022;20(7):409-423. doi: 10.1038/s41579-022-00846-2.

Schmid DA, Boettler T, Schemmerer M, et al. Mechanisms of long Covid and the path toward therapeutics. Cell. 2024;186(5):753-769. doi: 10.1016/j.cell.2024.01.004.

Allen JG, MacNaughton P, Satish U, et al. Schools need better ventilation to help keep SARS COV 2 in check. Time. 2022;Oct;1. Retrieved from: time.com/6206343/school…

Curtius J, Granzin M, Schrod J. Increasing ventilation reduces SARS COV 2 airborne transmission in schools: a retrospective cohort study. arXiv. 2022;2207.02678.

Clemens D, Neiterman E, McCaffrey B, et al. Air cleaners and respiratory infections in schools: a modeling study. Environmental Health Perspectives. 2023;131(7):77007. doi: 10.1289/EHP10793541.

Vermont’s Attendance Policies Punish Sick Kids & Their Families. FYI VT. 2024. Retrieved from: fyivt.com/be-informed/vt…

Petersen CJ. Did COVID teach us anything about school attendance? Medium. 2022. Retrieved from: medium.com/age-of-awarene…Image

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More from @Dave_it_up

Sep 10
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.

Let this be one of them.Image
Some Reading:
How Emotions Are Made, Lisa Feldman Barrett; lisafeldmanbarrett.com/books/how-emot…
Tooth and Claw Podcast, MeatEater; themeateater.com/listen/tooth-a…
The Loneliness of Illness, Psychology Today; psychologytoday.com/us/blog/the-gu…
The Burden of Invisible Illness, Harvard Health Publishing; health.harvard.edu/blog/the-burde…
In Sickness and in Health: The Psychology of Caregiving, National Institute on Aging; nia.nih.gov/news/sickness-…
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?
Read 4 tweets
Jun 23, 2024
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.Image
Sources
[1] COVID-19 Virus Can Persist in the Body More Than a Year after ...
[2] Long COVID: A proposed hypothesis-driven model of viral ... - NCBI
[3] Prevalence of persistent SARS-CoV-2 in a large community ... - Nature
[4] Viral persistence, reactivation, and mechanisms of long COVID - NCBI
[5] The persistence of SARS-CoV-2 in tissues and its association with ... biospace.com/article/releas…
ncbi.nlm.nih.gov/pmc/articles/P…
nature.com/articles/s4158…
ncbi.nlm.nih.gov/pmc/articles/P…
thelancet.com/journals/lanin…
Someone just let me know that there are actually two more studies that are important. I will post them as soon as I get a hold of them.
Read 6 tweets
Dec 24, 2023
Similarities of HIV and 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.

elifesciences.org/articles/84790
From Merk manual for healthcare professionals.
Image
Image
Also thanks for graphic @dbdugger
Read 4 tweets

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