The Coronavirus Exposed. Part 5: More Updates

photorandy2023

1 year ago

I have written several articles on the coronavirus and on masks. A series of links have been provided at the bottom of this article for your convenience. This article will, however address a different aspect of the virus or on healthcare issues in general.

I know COVID has been around a while, so now even my third part is acting very sluggish. So I will start a 5th installment. The previous three sections will remain all accessible for viewing, though they will now function as an archive. https://common-sense-in-america.com/2023/11/08/the-coronavirus-exposed-part-4-more-updates/. I am anticipating that this will most likely be my last installment in quite some time, as the updates are failry infrequent now.

Table of Contents

-COVID-19 can ruin your sleep in many different ways—here’s why

-COVID-19 can interfere with your period in many ways. Here’s how.

-Why does COVID-19 cause brain fog? Scientists may finally have an answer.

–We Indulged Our Child During COVID Lockdown. Did That Change Him?

–COVID Rates Are Rising Again. Why Does It Spread So Well in the Summer?

-What is POTS? This strange disorder has doubled since the pandemic.

–Long COVID Is Harming Too Many Kids

-Jury: Bay Area Transit Workers Fired for Refusing COVID-19 Vaccine to Get More Than $1 Million Each

–Confronting the Dangers of Silent Spread Is Necessary to Prevent Future Pandemics

COVID-19 can ruin your sleep in many different ways—here’s why

Scientists are learning more about the havoc that viruses and bacteria wreak on sleep. Here’s what you need to know about seeking care for insomnia.

(Update 11/16/2023)

Six weeks after a mild case of COVID-19 early in the pandemic, Erika Thornes started waking up every night between 2 and 3 a.m. Unable to fall back asleep, she would listen to podcasts, read, and scroll through Twitter before finally dozing off by 4 or 5 a.m. Thornes, the mother of three teenagers in San Diego, continued to struggle to sleep through the night for more than two years after that—a pattern that improved only after she started taking a new medication following her second bout with the virus in the summer of 2023.

A similar thing happened to her husband during a COVID-19 infection. He was suddenly waking up at 3 a.m. every night. His sleep improved when he stopped testing positive, but the symptom was extreme while it lasted. “He was quite shocked,” she says. “He knew I was waking up, but I don’t think he quite understood the severity of ‘awake.’”

Nightmares. Days without sleep. Waking in a panic in the middle of the night. Sleeping for 18 hours a day. As COVID-19 swept through the global population, so too did reports of sleep disruptions both during an infection and in the weeks and months beyond.

Studies published since the pandemic began have revealed new details about how the virus altered sleep and have documented the general ways that bacterial and viral infections interfere with sleep through physical and psychological mechanisms. New research has also revealed how poor sleep during and after COVID-19 can exacerbate many symptoms of both acute and long COVID—including brain fog—and how insomnia can lower production of antibodies after vaccination.

Recognizing the potential for SARS-CoV-2—the virus that causes COVID-19—to upset sleep, experts say, can help people get the care they need.

How sleep and the immune system affect each other

Sleep is intricately entwined with the immune system, a link both well-known and still mysterious. Getting enough rest can help prevent infections, according to evidence and observations going back thousands of years. But infections can also disrupt sleep in complicated ways.

Studies in animals show that viruses and bacteria alter both the amount of time spent sleeping and the kind of sleep, says John Axelsson, director of the Sleep Laboratory at Stockholm University’s Stress Research Institute in Sweden. When researchers inject rabbits or rodents with moderate doses of bacteria or viruses, the animals sleep more. They get more non-rapid eye movement sleep, a deep restful state thought to be important for recovery; and they spend less time in dream-filled REM sleep.

Cytokines, a category of molecules that can stimulate or slow down inflammation, appear to play a major role in these patterns, Axelsson says. When healthy animals are sleep deprived, levels of some pro-inflammatory cytokines in the brain rise, causing the animals to sleep more than usual. When scientists block these cytokines, animals don’t sleep more—even when they are sleep deprived.

It’s harder to do the same kind of research in people, and results are mixed about how sleep changes during illnesses. But studies suggest that, at least to some extent, inflammatory molecules affect sleep in ways comparable to other animals. In studies from the 1990s and early 2000s, researcher Thomas Pollmächer and colleagues injected people with bits of bacterial cell walls, called endotoxins, and found that mild activation of the immune system increased the drive for sleep and enhanced non-REM sleep.

But once the immune system revved up with increased cytokine levels and symptoms of illness, people experienced more disrupted sleep, not typically seen in animals. “The inflammatory system increases the drive for sleeping,” Axelsson says. “But at the same time, it then disrupts your sleep if you get a fever.”

To see how respiratory infections affect human sleep, Axelsson and colleagues recruited 100 healthy adults to keep a detailed sleep diary after experiencing the first symptoms of a respiratory infection while wearing a sleep-tracking device on their wrists. Of the 100 volunteers, 28 people got sick. Overall, those people spent longer in bed and slept more after their symptoms began, the researchers reported in 2019.

But this wasn’t a restful sleep. Infected people had difficulty falling asleep, woke up more, and had a more restless sleep especially when they were most symptomatic. As symptoms eased, sleep improved. Anecdotally, that’s the same pattern reported by many people with COVID-19—a lot of sleep initially followed by insomnia or other disruptions while sickest. The physiological drive to sleep more while getting sick might be adaptive—helping the body fight off the invader, Axelsson says.

Why sleep problems continue after COVID infection

For many people, sleep troubles don’t end on Day 10 or when a person tests negative. To gauge how often sleep troubles persist, researchers surveyed more than 650 long COVID patients who visited the Cleveland Clinic’s reCOVer Clinic between February 2021 and April 2022. Up to six months after an infection, 41 percent reported sleep disturbances; an additional 7 percent reported disturbances that were severe. Black patients, 12 percent of study participants, were three times more likely to report sleep problems compared with other groups—echoing disparities seen throughout the pandemic, says Cinthia Peña Orbea, a sleep specialist and lead author of the study, which was published in June.

Elsewhere, there have been reports of post-COVID-19 narcolepsy, excessive sleeping, and physically enacting dreams with movements like kicking and talking instead of lying still with typical sleep-induced paralysis, says Monika Haack, a psychoneuroimmunologist at Harvard Medical School in Boston, who co-authored a 2019 review of the links between sleep and disease.

Peña Orbea’s study suggests that long COVID-19 falls in line with other chronic illnesses for causing sleep issues. About 60 percent of people with HIV and more than 50 percent of people with hepatitis C experience poor sleep as do people with ME/CFS, also called chronic fatigue syndrome. People with inflammatory bowel disease, rheumatoid arthritis, and other inflammation-related diseases—all immune disorders—often suffer from lack of sleep.

Sleep disorders appear to be common after severe cases of COVID-19, according to new evidence. Among survivors who were admitted to the ICU, put on ventilators, or had extreme symptoms like a very low oxygen levels, a third had ongoing sleep disorders after recovering from their illness, found a 2023 review of 16 studies that included more than 10,500 people.

A direct link from insomnia to respiratory illness

Although getting a good night sleep has long been standard advice for staying healthy, there hadn’t been large studies to assess whether insomnia directly boosted the risk of getting sick, says Hanna Ollila, who studies sleep at the University of Helsinki and Massachusetts General Hospital. To fill the gap, she and colleagues turned to two databases containing health records from 558,000 people in Finland and the U.K.

Ollila’s team reported in 2023 that that a prior diagnosis of insomnia increased the later risk of developing an upper respiratory infection, influenza, and COVID-19. For COVID, the data suggested that insomnia made people more susceptible to developing severe illness rather than making them more vulnerable to infection. “The connection between sleep and infections has been a question in many earlier studies,” Ollila says. The new study, she says, helps draw a line from sleep disruption to risk of getting sick.

Again, inflammation appears to help explain the link. In a 2022 study, Haack and colleagues found that disturbing sleep in 24 healthy people led to the production of more molecules that prolonged inflammation and notably, a suppression of molecules that normally stop that inflammation. Even after three full nights of recovery sleep, inflammation persists, emphasizing the need to preserve good sleep in the first place.

Sleeplessness can cause or exacerbate many symptoms associated with both acute COVID and long COVID, including depression, fatigue, and brain fog. Those symptoms in turn can make it hard to sleep. “It’s always bi-directional,” Haack says. Insomnia, sleep apnea, and other disruptions, she says, “all can lower sleep quality, depth, continuity, or regularity, and dampen the immune supporting functions that come with normal sleep.”

Sleep is also important to get maximum benefits from vaccines, says Nikolaos Athanasiou, a pulmonologist at the University of Athens, Greece. Among 544 healthcare workers who hadn’t previously been infected with the SARS-CoV-2 virus, those with insomnia produced lower levels of antibodies in response to the COVID-19 vaccine. “It has not been pointed out enough,” Athanasious says, “that sleep deprivation and reduced sleep duration decreases immune response.”

Developing drugs for COVID-related sleep disorders?

Ultimately, scientists might be able to develop medications that affect levels of cytokines to improve sleep, says James Krueger, an expert on the biochemistry of sleep at Washington State University in Spokane. But it’s a challenging task because the relationship between cytokines and sleep are extraordinarily complex. Some pro-inflammatory cytokines enhance sleep at low concentrations but at higher concentrations, they lead to wakefulness and fragmented sleep. There are also anti-inflammatory cytokines that mostly inhibit sleep at low concentrations.

Hundreds of proteins interact to regulate the immune system and other processes, Krueger says. COVID-19 and other infections tweak those interactions. Targeting those molecules remains a work in progress. “For complex behaviors and brain processes such as sleep, some new drugs have been developed over the past few years,” he says. “Time will tell if they are better than prior drugs.”

The impact of psychological stress

A better understanding of how infections affect sleep in biological ways will develop with more trials and better data, Axellson says. In the meantime, a slew of studies suggests that stress, disruption in routines, mental health, and other non-physiological factors related to illness also affect sleep.

During lockdowns, 57 percent of people reported poor sleep quality, found a 2020 survey by Italian researchers. Overall, people spent a longer time in bed while quarantined, studies show. But they didn’t sleep as well as before they were confined to their homes and isolated from others, and their dreams became more vivid, bizarre, and emotionally intense.

For many people, those issues persisted even after lockdowns ended, as people started getting out more and feeling less stressed, Italian researchers reported in 2021. The researchers speculated that for many people—including children—psychological distress lingered past the acute phase of the pandemic. A 2023 study by researchers in Spain found that sleep quality declined during lockdowns among kids, ages 5 to 9. Like adults, their sleep hasn’t bounced back since, possibly because of ongoing anxiety and a persistent increase in screen time.

How to improve sleep after COVID-19

Helping people get better rest during and after COVID-19 infections begins with acknowledging the importance of sleep, Haack says. That can include avoiding medications that disturb sleep, such as opioids, and reducing light, noise, and repeated wakeups for people who are hospitalized.

Establishing regular sleep routines with consistent bedtimes and wakeup times are often a part of insomnia care, Axelsson says. It can also help for people to restrict time in bed to increase sleep efficiency and avoid excessive time spent lying awake.

Haack recommends mindfulness apps to reduce stress and anxiety. For her long COVID-19 patients, Peña Orbea has seen cognitive behavioral therapy led to improvements. “With insomnia, the brain is in a hyper-arousal state,” she says. “We try to reset that arousal state of mind.”

Physical activity and being outside in daylight can help a subset of people who may have stopped going out because of their illness, Axelsson says. But for many with long COVID, exercise can cause serious setbacks, underscoring the need for individualized medical care if sleep problems persist post-COVID.

“Sleep disruption can be quite normal during the acute COVID infection, due to sleep-disrupting symptoms such as pain, coughing, stuffy nose,” Haack says. “If sleep disturbances continue to stay beyond the acute symptomatic phase or start to develop as a new symptom, that is the time to seek help.”

COVID-19 can interfere with your period in many ways. Here’s how.

There could be temporary disruptions to your cycle after the vaccine—or more significant issues after a severe bout of COVID-19.

(Update 11/16/2023)

Raven La Fae, a 32-year-old artist in Calgary, Canada, has always been able to predict their menstrual periods almost to the day; it arrived every 28 days and lasted for five. But after contracting COVID-19 in late 2020, that’s no longer the case.

La Fae’s bout with the disease lasted for two miserable weeks. A menstrual cycle landed expectedly during that time, but what was shocking to them was how long the bleeding continued—10 days.

“My period has been funky ever since,” La Fae laments, and after another round of COVID-19 it became even less predictable. While the days between cycles have mostly returned to baseline, the number of days of bleeding have not, lasting up to 10 days a month.

From the beginning of the pandemic, women worldwide noticed changes to their menstrual cycles. In some cases, this happened after contracting the virus; in others, after receiving a vaccine. With so many people recording their cycles in period-tracking apps, researchers have been able to document the phenomenon.

Initially, many physicians were taken off guard. La Fae’s healthcare provider, after determining hormone levels were normal, said she couldn’t explain it. People complained their doctors dismissed their hunch the virus might be linked to disrupted cycles.

“When COVID started we were worried about people dying, so other things were overlooked,” admits Hugh Taylor, chair of obstetrics and gynecology at Yale Medicine. In retrospect, Taylor says, patients should have been alerted to this possibility. “We see irregular menstrual cycles with other acute infections, so it isn’t surprising it happens here.”

Poor messaging

Without research or reassurance from physicians, women were alarmed by the deviations in their periods, Taylor says, and for good reason: “We’ve been warning people for years that changes in a period might be a symptom of a hormonal imbalance, or even cancer.”

When girls and women noticed unexpected shifts in their cycle after receiving a COVID-19 shot, some second-guessed their decision to get a vaccine, says Candace Tingen, a program director at the National Institute of Child Health and Human Development, which awarded $1.67 million to five research institutions to study the issue.

Tingen points out that her institute has long emphasized the importance of menstrual cycles to health. “We talk about it as a fifth vital sign,” she says (the other four being body temperature, blood pressure, pulse, and respiration).

Most concerning to younger women was whether these changes could reduce fertility, Taylor says.

It wasn’t until early 2022—two years into the pandemic—that a study of 2,000 American couples published in the American Journal of Epidemiology resolved the question. Women trying to conceive who’d had the virus saw no decrease in fertility. Similarly, the COVID shot had no impact on conception rates.

Both virus and vaccine may temporarily alter menstruation

Several NIH-funded studies have confirmed that COVID does alters cycle lengths in many women, albeit only briefly.

Thousands of reproductive-age women using a period tracking app reported that the time between their periods expanded by more than a day in the month following infection or vaccination, which for most returned to normal the following cycle, researchers reported in August.

Another study of 127 women of childbearing-age in Arizona who had contracted COVID found 16 percent reported some alteration; most common were irregular cycles or longer gaps between bleeds. These shifts were more likely in those whose infection involved more symptoms or was more severe (but not to the point of hospitalization).

Women in this study also had increases in the premenstrual syndrome symptoms of mood changes and fatigue.

“We think of the menstrual period as an acute event that occurs for a few days, but hormones are changing throughout the entire cycle,” explains Leslie Farland, an epidemiology professor at the University of Arizona and the study’s principal investigator.

A large study published in June focused on COVID vaccinations confirmed that here too the number of days between periods increases by about a day during the month of vaccination, but returns to normal after.

That aligns with a prior study tracking 4,000 U.S. women who used one period tracking app and found that, for the vast majority of women, cycles shifted slightly and temporarily; however, the length of bleeding didn’t change, says Alison Edelman, an obstetrician and gynecologist at Oregon Health and Science University and the study’s principal investigator. A second study by Edelman, of nearly 20,000 women in North America and Europe using the same app reported similar findings.

Still, ten percent of the women in Edelman’s study saw their period shift by more than a week after getting the shot. However, these women were also largely back to normal the following month.

None of these studies explain situations like La Fae’s, where menstrual cycles are changed significantly and persistently.

How does coronavirus change a period?

Exactly how the coronavirus or vaccine affects the menstrual cycle isn’t clear.

One hypothesis posits that COVID-19 may affect what’s known as the hypothalamic-pituitary-ovarian axis. To begin each monthly cycle, the hypothalamus gland signals the pituitary gland to secrete two hormones that together release an egg from the ovaries.

It’s possible the coronavirus affects the hypothalamus directly, Taylor says, but the body may also proactively decrease the activity of these glands if the virus is detected. “This has evolutionary advantages, because you don’t want to get pregnant when you’re fighting off a physical stressor, which could be an illness or malnutrition or the like,” he explains.

Alternatively, the immune system engaged in fighting the virus could alter the normal inflammatory response of the uterine lining (endometrium) during the cycle.This may be why people who experienced a more intense bout of COVID—indicating a higher viral load and more immune activity—have higher rates of menstrual changes, as the University of Arizona study found.

That was the case for Annette Gillaspie, a 41-year-old registered nurse in Hillsboro, Oregon, who contracted COVID in 2020 and was extremely ill for more than two weeks. She has since experienced long COVID symptoms, including a fluctuating heart rate and fatigue so extreme a shower can send her to bed for days. Her periods are unusually long and heavy—gushing for almost two weeks some months—and even having a hormonal intrauterine device inserted didn’t reduce the bleeding as it normally does. At some point, she says, she’ll likely have to undergo a hysterectomy.

Vaccines trigger more minor shifts

Vaccines trigger the body’s immune system response, albeit a smaller one than the disease, so the same mechanisms could be involved in their temporary menstrual cycle disruptions, Tingen says.

Disseminating this reassuring information to women so they know to expect this possible side effect is an important public health task, Tingen says.

Anyone whose cycle remains significantly altered for several months, however, should check with their healthcare provider, Taylor says. “My suspicion is that people on the cusp of a medical condition—thyroid abnormalities, hormonal irregularities, bleeding from fibroids—might be pushed over the edge” by the coronavirus or COVID vaccine.

Edelman hopes this will be a teaching moment for her profession. “Menstrual health has been woefully understudied, not just in vaccine trials but in almost every area of research,” she says. “Yet half the population will, does, or has menstruated, and this routine biological function has meaning for the individual and for science.”

Why does COVID-19 cause brain fog? Scientists may finally have an answer.

Nearly 40 percent of long COVID patients suffer from the disorienting condition. Destroyed connections between brain cells may be to blame.

(Update 11/16/2023)

When scientists infected brain organoids—pinhead-size bits of brain tissue grown in the lab—with the virus that causes COVID, they found that not only does it spread in neurons in the brain, it also accelerates the destruction of connections between neurons—called synapses—that are essential for communication.

These discoveries expand understanding of how SARS-CoV-2 can damage the nervous system. COVID-19 patients continue to suffer with a range of symptoms, especially neural and behavioral problems, long after the infection. One such condition, commonly known as brain fog, causes disorientation, memory loss, chronic headache, and numbness, and it affects nearly 40 percent of long COVID patients.

“There are many case reports, even some in our own clinic, of patients who have symptoms [of brain fog] lasting upwards of a year,” says Ayush Batra, a neurologist at Northwestern University Feinberg School of Medicine.

Carl Sellgren, a psychiatrist and cellular biologist, and his team at the Karolinska Institute in Sweden used organoids to study what SARS-CoV-2 does to brain.

“It was quite striking that very small amounts of the virus could quite rapidly spread in the organoids and eliminate an excessive number of synapses,” says Ana Osório Oliveira, a neuroscientist in Sellgren’s team.

Another study found that spike protein—which coats the outer surface of the virus—directly eliminates synapses causing loss of memory in lab mice by causing inflammation.

Destroying too many connections between neurons, or over-pruning, may be causing brain fog in long COVID patients. “This could be one of the many reasons—probably—why we are observing a range of neurological symptoms, even after the infection is long gone,” says Samudyata, a postdoctoral researcher at Karolinska Institute who led the study and only uses one name.

Virus has been found in autopsied brain tissues and throughout the bodies of patients, who died more than 200 days after contracting COVID-19. It is evidence that the virus is capable of persisting in organs throughout the body.

“There are some persistent virus reservoirs that can cause a chronic inflammatory response or autoimmune attack on the brain, which can cause pruning and brain shrinkage,” says Batra.

Pruning connections between neurons is essential for learning

The brain is made of a dense and dynamic network of nerve cells that communicate through synapses that change as humans learn. “Synapses are essentially how cells talk to each other and how information is passed from one part of the brain to another,” Lancaster says.

Synapses are responsible for all the functions of the brain, from memory to controlling movement to feeling emotions, and they are constantly remodeled. “That’s how we learn,” she says.

The junctions between neurons that talk to each other frequently have more knob-shaped synapses that produce neurotransmitters—chemicals that transmit signals to other neurons. Conversely, neurons that communicate less or not at all have fewer synapses because they are removed, or pruned, by immune cells called microglia. Microglia make up to 17 percent of the cell population in some parts of the human brain and perform housekeeping duties by migrating through the brain eating dead cells and scavenging weak synapses.

Although synaptic pruning is most active in developing brains such as in fetuses and infants, it continues in healthy brains throughout life and is necessary for encoding new memories and erasing the ones it no longer needs. Synaptic pruning is also critical for the brain to recover from an injury; allowing it to strengthen synapses which relearn the lost skills and remove synapses that no longer function.

Using brain organoids to study neural damage

Studying a direct link between COVID-19 and cognitive dysfunction, such as brain fog, is difficult in living brains. That is why studies are often limited to cadavers of COVID-19 patients. But brain organoids, often called mini-brains, allow scientists to see in real time how SARS-CoV-2 affects living tissue.

Mini-brains can be used to study infection because scientists can control the amount of viruses that are exposed to individual cells, says Oliver Harschnitz, group leader in the Neurogenomics Research Centre at Human Technopole Institute in Milan, Italy, even though tissue organization is less structured than real brains.

Using brain organoids, Oliveira and her colleagues found that the virus itself was not directly pruning the synaptic connections but was activating the microglia.

“We found that following infection by SARS-CoV-2, somehow the microglia become immunoreactive, and eat more of the synapses than normal,” Samudyata says.

It’s a very interesting study because it really shows the quantitative differences in the microglial activity after COVID-19 and its effect on synapses says Ayush Batra, a neurologist at Northwestern University Feinberg School of Medicine.

Too much synapse pruning can be detrimental and has been linked to neurodevelopmental disorders such as schizophrenia, as well as neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases.

In a follow-up study, Sellgren’s team has found that a protein called C4A—which helps remove microbes and infected cells—also tags synapses for removal. Although his research doesn’t directly connect C4A with brain fog, it suggests that inflammation after infection can affect pruning of synapse, depending on genetics, says Sellgren.

If the excessive elimination of synapses that occur in brain organoids after SARS-CoV-2 infection also occurs in people, it may destroy vital connections and explain why some with COVID-19 suffer from long-term neurological symptoms.

“Too much synapse elimination would be expected to affect a person’s ability to form new memories, or to remember existing ones, and could help explain the sluggish brain functions seen in brain fog,” Lancaster says.

This is consistent with studies done at the U.S. National Institutes of Health that have found antibodies produced in response to SARS-CoV-2 can attack the cells lining the brain’s blood vessels, causing damage and inflammation—which activates microglia—even if the virus doesn’t directly enter the brain. That may explain why, as Batra’s team has shown, some long COVID patients not sick enough to be hospitalized continue to experience neurologic symptoms beyond a year after initial infection.

Is the loss of synapses causing brain shrinkage?

A U.K. study has also shown that even mild COVID-19 can shrink the brain through loss of gray matter—the outermost layer of the brain that is vital for controlling movement, memory, and emotions—causing physical changes equivalent to a decade of aging. A new study, which has not yet been peer-reviewed, suggests that COVID-19 can accelerate the decline of cognitive ability equivalent to ten years of normal aging, especially after severe COVID disease or severe long COVID.

“We are still unclear what may contribute, in general, to a loss of gray matter volume or thickness observed using MRI,” says Gwenaëlle Douaud, a neuroscientist at the University of Oxford who led the study.

While synapse elimination, as shown in Samudyata’s study, could account for a small percentage of the change in the gray matter, says Douaud, more studies combining imaging with tissue sections are required to determine the other factors that lead to brain shrinkage.

Hyperactive microglia may cause problems in other ways. The Swedish study also shows that the pattern of genes turned on and off by the microglia in brain organoids after SARS-CoV-2 infection mimicked gene activity seen in neurodegenerative disorders. This may explain why there is a three times higher risk of developing neurological or psychiatric conditions within six months after COVID-19 compared with those who were not infected. In adults aged over 65, the risk of developing dementia after a COVID-19 infection is almost twice that of other respiratory infections.

However, scientists caution that much more research is needed to understand the effect of SARS-CoV-2 infection on the brain. As organoids resemble immature cells—like those in a fetal or post-natal state—this limits extrapolation of the results to mature adult brain cells.

“While these data are exciting and indicate a role for proinflammatory microglia in the disease mechanisms underlying long COVID, more studies are required to validate these findings and build on them,” Harschnitz says.

It’s also not known how long COVID affects quality of health and whether it has long term or irreversible effects on the brain. So as the pace of holiday and indoor winter activities picks up, Samudyata advises taking preventative measures and staying up to date on vaccinations to minimize the chance of getting COVID over and over. While it isn’t clear how the virus exerts detrimental effects on the brain, it’s evident that it does cause damage.

We Indulged Our Child During COVID Lockdown. Did That Change Him?

(Update 7/10/2024)

There was a time when my wife Emily and I spoiled the heck out of our son.

He was our first child and just two years old when COVID restrictions sent nearly everyone into lockdown. Because we were trying to have another, and Emily’s elderly father lived under our care, we spent most of the first half of my son’s second year alone at home.

We did our best to keep him sated with games and his few buckets of toys. We relied heavily on screen time to keep him occupied while Emily and I did our best to keep our careers afloat. We took countless walks in the woods behind our house, playing in the knee-high water of the small, clear creek that runs past our neighborhood.

As COVID measures started to lift, daycares and kids’ museums in our town were still closed, and playdates ever tricky, as coordinating and maintaining everyone’s level of comfort was a feat unto itself.

Considering everything he had endured and his general state of isolation, Emily and I bought our son a little gift nearly every time we left the house, figuring it was one of the few ways we could keep him happy, engaged and entertained in such an unprecedented time.

It was never anything more than tossing a $1 Hot Wheels car into a shopping cart already piled with at-home COVID tests and N95 masks at the local pharmacy. After all, there are only so many hours of Frozen a little boy can watch each day (roughly five, empirically speaking). This went on through the end of summer, until he was able to start daycare. Though we slowly weaned the process down from every time we left the house to once a week or so, Emily and I suspected we might be doing some lasting harm to our son, creating a little boy who expected gifts every time one of us left the house.

As time went on—and with the help of the amazing caregivers at his daycare program—Emily and I began to untangle this idea. Yet, four years later, Emily and I occasionally see remnants of that “spoiled” little boy, often manifested in selfishness. Though those moments are growing fewer and further between, owing much to his experience of becoming a big brother, our son will still pout or occasionally have an outright meltdown when met with a firm “no,” especially if a new toy is involved. He’s quicker to recover now that he’s getting a bit older. But are these tantrums perfectly normal, or are they because Emily and I spoiled him during the lockdown era?

As he is our firstborn, everything our son does is new to us—we don’t really know what normal is. Is our son forever changed because of the pandemic lockdown or is he now just an average six-year-old; a kid who is figuring out the world around him while displaying some very standard selfishness?

While much of the research on COVID-related isolation is ongoing, in general, isolation isn’t good for children. Social isolation in childhood—when kids are excluded or report feeling lonely —can lead to depression, problems in school, a bleaker outlook on careers, increased body weight and even heart disease.

But as we are now a couple of years out from the lockdown part of the pandemic, some trends are starting to emerge. A study conducted by Columbia University researchers and their colleagues found that babies born at the beginning of the pandemic had slightly poorer social and motor skills at age six months than babies born just before the pandemic.

Another study published in JAMA Pediatrics last year found that children who were exposed to the pandemic between the ages of one and five were “4.39 months behind in development” at age five “compared with those not exposed to the pandemic.” And yet another study, also published last year in JAMA, found that young children exposed to the pandemic were more likely to experience socioemotional delays compared to children in the pre-pandemic era.

As I read through this research, elements like “increased emotional symptoms and self-regulation difficulties” shot out at me. Was my son experiencing such an increase? Did he have issues self-regulating? Or was he, again, progressing as normal? It’s impossible not to wonder. And though the generation of young kids who spent a few months in isolation is hardly an apples-to-apples comparison to children who have had severe and protracted bouts of isolation, it’s hard to keep my parenting brain from straying to the worst-case scenario. After all, it’s often what the parenting brain is programmed to do.

I’m heartened by the fact that my son is beginning to show greater signs of selflessness. He’s always been quick to share his toys, but now my wife and I are noticing how much more readily he accepts no for an answer. I’m also curious to know how much of that has to do with the normal development of a child, as studies have shown it’s around age six that kids begin to shed some of their childhood self-centeredness, to develop more empathy for people and the world around them. It’s at this age, my son’s age, that children’s executive function skills mature, which allows them to better manage their own distress and recognize the feelings and needs of those around them. And so, according to that metric, our little boy is right on schedule. Still, even if he is progressing emotionally, I have to assume that six months of lockdown has left some kind of an imprint on him.

Almost 15 million children were born in America between 2017 and 2020, and 90 percent of brain development occurs before kindergarten. The idea that the world might have a microgeneration of lockdown babies is hardly a stretch. It’s not clear how that will manifest. Ongoing research will hopefully answer these questions once and for all.

But, knowing what we know, I think we can remain hopeful—kids who were in isolation for six months won’t have the same outcomes as children who have been isolated longer or more frequently. Considering as much, the best we can do is hope ongoing research shows that the long-term effects of the pandemic isolation were minimal.

During lockdown, everyone had struggles. For people like me and Emily, parents of young children, it was juggling jobs and new parenthood while trying to keep our baby happy, occupied and developmentally safe and sound. In the end, we did what we had to do to make it to the end of the day in one piece. We indulged our son, knowing full well it might have long-term effects. Now, as we move forward through his life, we are trying to be attuned to his development, to support him and help him thrive in any situation, and, of course, to help him get more comfortable with being told “no.”

COVID Rates Are Rising Again. Why Does It Spread So Well in the Summer?

A combination of human behavior and immunity, the environment, and SARS-CoV-2 itself explains why the virus surges during both hotter and colder months

It’s that time of year: a thick, oppressive heat blankets everything, people huddle inside air-conditioned homes, offices, shops and cafes for respite—and COVID is surging again.

Levels of SARS-CoV-2, the virus that causes COVID, have increased in wastewater samples across the U.S., with the biggest uptick in the West. The percentage of positive tests—though not a perfect metric because people aren’t testing as much—has also increased, but hospitalizations have remained relatively low. Most viral respiratory infections, such as influenza, peak in the winter. But for the four years that SARS-CoV-2 has circled the globe, it has caused peaks not just in winter but every summer, too. The question is, why?

Amanda Montañez; Source: Centers for Disease Control and Prevention

Possible reasons for the summer COVID peak are complex, but they fall into three main categories: characteristics of the virus itself, characteristics of its human hosts, and environmental factors.

SARS-CoV-2 continues to evolve new variants. One rises to the fore every six months or so, according to Peter Chin-Hong, a professor of medicine at the University of California, San Francisco, who specializes in infectious diseases. In recent weeks several new subvariants of the virus’s Omicron variant have emerged as dominant—including the so-called “FLiRT” variants (such as KP.2 and KP.3), as well as a newer variant called LB.1. These variants may be slightly more transmissible or better at evading the immune system than previous ones, Chin-Hong says.

Human behavior and the environment are other likely drivers of summer surges. During the summer, many people gather for events, travel for vacations or simply spend more time inside to beat the heat. The Northern Hemisphere winter has a string of holiday gatherings that are perfect for spreading disease; likewise, “in the summer, it’s Father’s Day, graduation, Fourth of July and then summer travel,” Chin-Hong says. “It’s kind of a like a one-two-three punch.”

“We know that nearly all [COVID] transmission happens indoors, in places with poor ventilation and/or poor filtration,” says Joseph Allen, an associate professor at the Harvard T.H. Chan School of Public Health and director of the Harvard Healthy Buildings Program. “One hypothesis is that these building factors and human behavior are driving the summertime increases in cases.” Although many offices or other large buildings have an HVAC system that can pull in fresh air from outside, many houses and apartment buildings with window-mounted air conditioners do not. Instead these ACs simply recirculate stale, virus-laden air inside a room.

Some studies have shown that humidity and temperature can also affect SARS-CoV-2 transmission. The virus is thought to survive best when humidity and temperature are low because cool and dry air holds less moisture—so virus-trapping microscopic droplets can remain airborne longer before settling on the ground. But these factors are probably less significant than human behavior and the characteristics of SARS-CoV-2 itself. Early in the pandemic, scientists thought summer might slow COVID because the virus is exposed to higher heat and more solar ultraviolet light.“ But look at Florida and tropical countries,” Chin-Hong says. “There was no break.”

It’s a persistent mystery why COVID spreads so efficiently in the summer as well as winter, whereas flu tends to be mostly a winter disease, says Linsey Marr, a professor of civil and environmental engineering at Virginia Tech, who specializes in aerosol transmission of pathogens. “I’ve studied the seasonality of the flu for many years, and we have some hypotheses about why it peaks in the wintertime,” Marr says. One is that the flu virus survives better in dry conditions. Another is that our immune system is weaker in winter, and a third is that heated buildings are tightly sealed and recirculate contaminated air. In the summer, some of these conditions apply in cool, air-conditioned buildings—yet we don’t see a summer flu peak. SARS-CoV-2 appears to be hardier than the flu virus, Marr notes, so it might simply be able to survive conditions that flu can’t.

With climate change bringing more frequent and severe heat waves to much of the U.S. and the world, people will likely be spending even more time indoors in summertime—and so will SARS-CoV-2. This year’s summer surge appears to have started on the West Coast, which has already had several weeks of severe heat.

And then there’s the human immune system. People’s immunity to COVID may have waned since the last time they were vaccinated or infected in the fall or winter, making them more susceptible to getting sick. Fortunately, immunity from past exposure, in the form of memory T cells, keeps most people from getting severely ill. But waning antibodies mean people can still get infected.

Earlier this year the U.S. Centers for Disease Control and Prevention encouraged people aged 65 and older to receive a second booster of last fall’s COVID vaccine. But fewer than a quarter of adults have even gotten a first booster since last fall. Chin-Hong recommends that if you haven’t been vaccinated in the last year, you should do so now. Older adults—especially those who are immunocompromised, planning a trip or attending a large gathering such as a wedding—should consider a second booster, too. And the Food and Drug Administration recently authorized a new version of the vaccine for the fall that is targeted toward the FLiRT variant KP.2 or its predecessor, JN.1.

Of course, there are other steps people can take to avoid summertime COVID, and many of them will sound familiar: masking, breathing cleaner indoor air by increasing ventilation and filtration, and avoiding crowded indoor spaces.

Today, four years since COVID first emerged, most people have some level of immunity to SARS-CoV-2 through vaccination, infection or both. And the virus is not nearly as deadly as it once was (although it still poses a danger to chronically ill or immunocompromised people, and long COVID is always a risk). At this point, Allen says, we’d be better off finding more structural solutions, such as redesigning buildings to allow for both climate control and clean, healthy air, instead of having to choose between them. “We’ve been fed this false narrative that it’s energy efficiency or healthy indoor air,” Allen says. “I reject that. And everyone should reject that. We can have both.”

What is POTS? This strange disorder has doubled since the pandemic

(Update 8/3/2024)

Millions of people now live with the debilitating disorder, which can be triggered by viral illnesses like COVID-19. And many say the recommended treatment—exercise—has backfired.

In late 2021, after 18 months of long COVID symptoms, Oonagh Cousins, a member of Great Britain rowing team, was ready to resume training. She’d contracted COVID-19 in early 2020, and although her initial case was mild, Cousins spent the next year and a half experiencing a fatigue that went far beyond just feeling tired. “It was like a deep sickness,” she says, a “sludgy, deep weakness” that flared up after even mild exertion.

After that lengthy recovery period, Cousins’ only remaining symptom was a very mild case of postural orthostatic tachycardia syndrome—POTS—which is a type of dysautonomia characterized by an abnormal rise in heart rate after changing position, like sitting to standing. Patients with POTS report a variety of symptoms, including dizziness, fatigue, brain fog, and gastrointestinal disturbances.

Cousins is among millions of people living with POTS, a number that is estimated to have doubled since the beginning of the pandemic. She’s not the only elite athlete with the disease either: U.S. Olympic swimmer Katie Ledecky revealed in her new memoir that she is also living with the condition. Some of the known triggers include pregnancy, surgery, or a viral illness, such as COVID-19. A subset of these POTS patients also has a condition called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is characterized by post-exertional malaise (PEM)—a situation in which symptoms worsen after exercise.

For patients with PEM, pushing past their physical limits—often encouraged in POTS recovery exercise protocols—can lead to major crashes. As a result, many patients with POTS and ME/CFS report being given inappropriate guidance on exercise, the consequences of which can be severe.

“They don’t teach us about ME/CFS or POTS in medical school,” says Sujana Reddy, a resident physician at East Alabama Medical Center, who developed both conditions after a COVID-19 infection in 2020.

Exercise and POTS

When Cousins felt ready to resume her training, she consulted with her doctors, who told her that the cure for her dysautonomia was exercise. With their approval, Cousins eased back into training, with three workouts a week.

After a full year of training, she had a major relapse, her dysautonomia having gone from mild to severe, which she attributes to over-training. “It was basically an accumulation of dysautonomia and post-exertional malaise,” Cousins says. As she and many other POTS patients are discovering, the relationship between exercise and dysautonomia is more complicated than the research suggests.

According to a recent estimate by the CDC, six percent of American adults are currently living with long COVID symptoms. With an estimated 79 percent of long COVID patients meeting the criteria for POTS, patients and healthcare practitioners are finding it necessary to re-evaluate how exercise fits into management of the condition.

Although exercise is considered to be a first-line treatment for POTS, in a survey of long COVID patients 89.5 percent of patients reported relapses after exertion, while other patients report difficulties with following some of the exercise protocols. As a result, the National Institute of Health and Care Excellence cautions against using graded exercise therapy for treating post-COVID fatigue.

For POTS patients whose condition wasn’t triggered by a COVID-19 infection, exercise can be helpful, but as many have discovered, it’s not a cure, nor is it an effective first-line treatment.

As a recent study has shown, although the majority of POTS patients use non-pharmaceutical treatments, such as exercise, to manage their symptoms, they are not as effective as pharmaceutical treatments. Still, many patients report being expected to prove that exercise alone is not enough to treat their symptoms, before their doctors will consider putting them on medication.

“A lot of doctors think that salt, fluid, and exercise is the only treatment patients need,” says Lauren Stiles, the founder of Dysautonomia International and a research professor in neurology at SUNY Stony Brook, who developed POTS in 2010. “That is very outdated thinking.”

When exercise backfires

As a number of studies have shown, exercise can decrease POTS symptoms, by making the heart more efficient and encouraging the body to produce more blood. In POTS exercise protocols, patients start with cardio in a recumbent position, such as rowing, swimming, or a recumbent bike, which helps avoid triggering symptoms by avoiding an upright position. Patients also do strength-training, which helps return blood to the heart more efficiently.

However, just as with any medication, there are nuances to the benefits of exercise, whether it’s figuring out the right amount and intensity, or screening for conditions that are often associated with POTS, for which exercise may be contraindicated. For other conditions, such as ME/CFS, exercise can lead to debilitating crashes.

For one of the major studies examining the effect of exercise on POTS symptoms, of the 103 patients who finished the three-month Levine exercise protocol, 71 percent no longer met the criteria for the disorder. However, the study had a 60 percent drop-out rate, with only 103 of 251 enrolled participants completing the protocol. The study also excluded patients who had other conditions, such as autoimmune disorders, that are often found in POTS patients.

“It’s rare for me to find a patient who gets referred to me with POTS, who doesn’t also have other comorbid conditions, such as hypermobility,” says Clayton Powers, a physical therapist at the University of Utah, who specializes in treating patients with POTS.

Fitting their own needs

Some patients have found POTS exercise programs to be useful, but only if they progress at a rate that is much slower than suggested and only if they add in medication.

For Stiles, who was a competitive snowboarder before developing POTS, exercise did not relieve her symptoms. However, after she was diagnosed and treated for an autoimmune disorder, which included regular infusions of intravenous immunoglobulin, “I went from bedridden to ice skating,” Stiles says. “Medication allowed me to very slowly work my way back into being an athletic person.”

A number of POTS patients, including many long COVID patients, also meet the criteria for ME/CFS, the hallmark symptom of which is post-exertional malaise. PEM is often characterized by a flu-like feeling, such as swollen lymph nodes, joint and muscle aches, and low-grade fevers that develop within hours and days following over-exertion.

“My world as a clinician is broken down into ‘Do you have post-exertional malaise or do you not have post-exertional malaise?’” says Todd Davenport, a physical therapy researcher at the University of the Pacific. “It’s a very important clinical decision point.”

Reddy, the resident physician in Alabama, spent the early months of her illness pushing through, only to progressively get worse. Eventually, at the urging of her doctors and family, she started physical therapy, only to experience a major crash, which left her bedbound for a month, unable to tolerate even minor stimuli such as light or sound.

For Whitney Fox, who was diagnosed with ME/CFS and POTS in 2019, even small amounts of exercise pushed her into a cycle of over-exertion followed by crashes, during which she was barely able to get out of bed. “I kept trying and trying, and I kept getting worse and worse,” Fox says.

For Lindsay Levinson, a long COVID patient with POTS and ME/CFS, understanding her new limits on exertion has been a steep learning curve, one that goes against all her former instincts. “I’m good at pushing myself,” she says. At the recommendation of her doctors, Levinson tried resuming her spinning classes, which had been her favorite activity before getting sick. After a month of doing once-a-week classes at a gentle pace, she had a massive relapse, characterized by full-body pain, and an inability to complete simple chores, such as bathing or cooking dinner.

Relapsing also kept Cousins housebound for months. After receiving treatment that includes medication, she’s been able to return to a more functional life with some gentle exercise, such as swimming laps or going for walks. “I’m trying to listen to my body, and do what my body asks for,” Cousins says. “I just want to be able to find a way to have a happy, healthy relationship with exercise, that makes me feel good.”

Long COVID Is Harming Too Many Kids

Pediatric long COVID is more common than many thought, and we keep letting kids be reinfected with new variants

Since the COVID pandemic began, claims that the disease poses only minimal risk to children have spread widely, on the presumption that the lower rate of severe acute illness in kids tells the whole story. Notions that children are nearly immune to COVID and don’t need to be vaccinated have pervaded.

These ideas are wrong. People making such claims ignore the accumulating risk of long COVID, the constellation of long-term health effects caused by infection, in children who may get infected once or twice a year. The condition may already have affected nearly six million kids in the U.S. Children need us to wake up to this serious threat. If we do, we can help our kids with a few straightforward and effective measures.

The spread of the mistaken idea that children have nothing to worry about has had some help from scientists. In 2023 the American Medical Association’s pediatrics journal published a study–which has since been retracted—reporting the rate of long COVID symptoms in kids was “strikingly low” at only 0.4 percent. The results were widely publicized as feel-good news, and helped rationalize the status quo, where kids are repeatedly exposed to SARS-COV-2 in underventilated schools and parents believe they will suffer no serious harm.

In January 2024, however, two scientists published a letter with me explaining why that study was invalid. Some of the errors made it hard to understand how the study survived peer review. For example, the authors claimed to report on long COVID using the 2021 World Health Organization definition, but didn’t properly account for the possibility of new onset and fluctuating or relapsing symptoms, even though that definition and the subsequently released 2023 pediatric one emphasize those attributes. Any child with four symptom-free weeks—even nonconsecutive ones—following confirmed infection was categorized by the study authors as not having long COVID.

In August, the authors of the study retracted it. They did not admit to the errors we raised. But they did admit to new errors, and said these mistakes meant they understated the rate of affected children.

And that rate, according to other research, is quite high. The American Medical Association’s top journal, JAMA, in August published a key new study and editorial about pediatric long COVID. The editorial cites several robust analyses and concludes that, while uncertainty remains, long COVID symptoms appear to occur after about 10 percent to 20 percent of pediatric infections.

If you’re keeping score, that’s as many as 5.8 million affected children in the U.S.—so far. And we know studies and surveys of adults have found that repeat infections heighten the risk of long-term consequences.

The JAMA study comparing infected and uninfected children found that trouble with memory or focusing is the most common long COVID symptom in kids aged six to 11. Back, neck, stomach and head pain were the next most common symptoms. Other behavioral impacts included “fear about specific things” and refusal to go to school.

Adolescents aged 12 to 17 reported different leading symptoms. Change or loss in smell or taste was most common, followed by body pains, daytime tiredness, low energy, tiredness after walking and cognitive deficits. The study noted that symptoms “affected almost every organ system.” In other words, these symptoms reflect real physiological trauma. For example, SARS-COV-2 can cause or mediate cardiovascular, neurological and immunological harm, even increasing the relative risk of new onset pediatric diabetes when compared with other lesser infections.

Children in schools today are often described as struggling with emotional regulation, attention deficits and developmental problems. Adolescents have some of the worst standardized test scores in decades. Pandemic measures such as school closures—most of which were short-lived and occurred several years ago—have been blamed almost entirely for children’s present-day behavioral and learning problems.

While it is clear these early pandemic disruptions negatively impacted many children, the unproven notion that “the cure was worse than the disease” has become dogma and sometimes involves reimagining history. For example, the Canadian Pediatric Society’s most recent COVID vaccination guidance fails to even acknowledge the existence of pediatric long COVID, while stating without evidence in its preamble that children were more affected by pandemic disruptions in activities than direct viral effects. It’s hard to imagine how this wording could encourage pediatricians and parents to vaccinate children against a disabling virus.

Consider also a small but widely publicized Bezos Family Foundation–funded study which unscientifically claimed accelerated cortical thinning, a type of brain restructuring that occurs over time, is caused by “lockdowns.” The study design could not demonstrate cause and effect, however, but only correlation. Pediatric brain experts have critiqued the research, pointing out that “no supporting evidence” was provided for the claim cortical thinning is from social isolation, and that it isn’t necessarily pathological. “Lockdowns” were neither defined nor controlled for in the study, which relied on 54 pandemic-era brains scans from different children than the prepandemic scans they were compared to—meaning there was no measurement of brain changes in specific individuals. The pandemic-era scans came from months when relevant CDC seroprevalence data estimate that the number of children with one or more infections rose from about one in five to around three in five. We might reasonably predict that many of the studied brain scans were therefore from children who recently had COVID.

It is understandably disturbing to entertain the idea that we might currently be recklessly allowing millions of children to be harmed by preventable disease. That may be part of why problematic studies such as these have gotten headlines. It is more disturbing, however, that almost no public attention has been given to infection itself as a potential cause of children’s behavioural and learning problems.

This makes no sense. We know that COVID harms the brain. Neuroinflammation, brain shrinkage, disruption of the blood-brain barrier and more have been documented in adults, as have cognitive deficits. These deficits have been measured as equivalent to persistent decreased IQ scores, even for mild and resolved infections. Millions of people have, or have experienced, “brain fog.” What, then, do we guess a child’s COVID-induced “trouble with focusing or memory” might be?

When you put together the estimate that 10 to 20 percent of infected kids may experience long-term symptoms, that many of the most common symptoms affect cognition, energy levels and behavior, and that children are being periodically reinfected, you have a scientific rationale to partly explain children’s widely reported behavioural and learning challenges.

We can do something to protect our kids. We can vaccinate them every season, which somewhat reduces the risk of long COVID. We can keep sick children home by passing laws that create paid sick leave and end attendance-based school funding. We can normalize rather than vilify the use of respirator masks that help prevent the spread of airborne diseases.

Finally, we can implement fantastic new engineered indoor air quality standards designed to greatly reduce the spread of germs. Clean indoor air should be expected as a right, like clean water. The cost of providing cleaner indoor air is low relative to the economic benefits, which even when conservatively modeled are in the tens of billions annually in the U.S. and more than ten times the costs. These costs are also small compared to the price children and their families would pay in suffering as a result of preventable long-term impairment.

By regulating, publicly reporting and periodically inspecting building air quality, similarly to how we oversee food safety in commercial kitchens, we can greatly reduce the spread of disease and reap huge benefits for everyone—especially children.

Jury: Bay Area Transit Workers Fired for Refusing COVID-19 Vaccine to Get More Than $1 Million Each

(Updated 10/28/2024)

At issue is a vaccine mandate for BART workers in San Francisco that was imposed in 2021.

Rail transit officials in California’s Bay Area have been ordered to pay more than $7 million to transit workers who were fired because they refused to get a COVID-19 vaccine years ago.

On Oct. 23, a federal jury in the U.S. District Court for the Northern District of California sided with six former San Francisco Bay Area Rapid Transit (BART) workers who had refused to get the vaccine for religious purposes.

BART was ordered to pay the group more than $7.8 million, with each individual receiving between $1.2 million and $1.5 million, the Pacific Justice Institute, which represented the transit workers in the trial, said in a statement on Oct. 24. The institute, a law firm representing the six former employees since 2022, said the eight-person jury deliberated for two days this week before returning the verdict that awarded the employees the compensation.

About a week ago, the federal jury also determined that BART had failed to prove that it suffered an undue hardship by denying accommodations to the ex-employees in the case.

On Oct. 23, the jury further found that the six employees met the burden of showing that there was a conflict between their religious beliefs and the BART vaccine mandate, which was implemented in 2021.

According to the law firm, the jury also agreed with the figures that the plaintiffs had provided for lost wages that they had suffered after losing their jobs. The jury then added $1 million each to those figures, the firm said, describing the verdict as a “legal earthquake.”

“The rail employees chose to lose their livelihood rather than deny their faith. That in itself shows the sincerity and depth of their convictions,“ Kevin Snider, the Pacific Justice Institute’s chief counsel, who served as lead trial attorney, said. ”After nearly three years of struggle, these essential workers feel they were heard and understood by the jury and are overjoyed and relieved by the verdict.”

The law firm stated: “During the trial, jurors heard compelling testimony from dedicated employees. One of the plaintiffs had worked for more than 30 years for BART, with a stretch of 10 years perfect attendance, before being unceremoniously dismissed. Another had been out on workers comp for months, with no scheduled return date, when she was fired.”

Lawyers for BART argued that multiple employees who had conflicts with receiving the vaccine had secular—rather than religious—reasons. But the jury disagreed with those arguments, the Pacific Justice Institute said.

The vaccine mandate was approved by BART’s board of directors in October 2021 and stipulated that all employees must get the COVID-19 vaccine. It allowed some employees to be exempt from the vaccine, including for religious reasons.

A year later, BART employees filed a class-action lawsuit accusing the operator of denying religious accommodations in violation of state law.

U.S. District Judge William Alsup, who presided over the lawsuit against BART, ruled that the operator’s policies did not violate the employees’ right to religious freedom, according to an order he issued in March.

A separate order issued by Alsup in January found that BART received 188 requests for a religious exemption and accommodation, and of that figure, 40 chose not to complete the process. They were either terminated from employment or ultimately got the vaccine.

“Plaintiffs’ putative class fails because its members have little in common beyond their request for religious accommodation,” the judge further said in his order. “They do not share a common religious objection. They do not share a vocation or a set of contractual rights. They do not present a similar set of potential accommodations and associated burdens. They do not present similar health and exposure concerns.

“Potential accommodations do not impact the same pool of coworkers. Those coworkers do not have the same bargained-for rights.”

The Epoch Times contacted BART for comment on Oct. 25 but received no reply by publication time. The rail operator’s spokesman, James Allison, told local news outlet SFGate that it had “no comment” on the verdict.

Confronting the Dangers of Silent Spread Is Necessary to Prevent Future Pandemics

We need targeted public health interventions to reduce transmission from asymptomatically infected individuals. Like COVID, silently spreading pathogens can lead to far more infections and fatalities

The telltale runny nose of a common cold, or the fever and aches associated with the flu, mark the way we classify respiratory illnesses—with their symptoms. Public health messaging relies on these symptoms, urging those who are symptomatic to stay home and avoid others. That makes sense. It reduces the risk that one case becomes many.

But what if transmission is not necessarily linked to symptoms? COVID has shown that diseases can lead to catastrophic societal harm when they spread without symptoms. Hence, preventing future pandemics requires greater investment in targeted public health interventions to reduce transmission—including from infected individuals who feel fine.

Indeed, asymptomatic transmission was essential to COVID’s transition from a fast-moving outbreak in Wuhan, China, in early 2020 into a global pandemic that led to more than one million reported fatalities in the U.S. by May of 2022. People who felt fine transmitted their infection to others before developing symptoms (during a presymptomatic phase) or even if they never developed symptoms. Comparisons of early outbreak data revealed that approximately half of infected individuals were asymptomatic. That would be good news if asymptomatic infections were nontransmissible. But that wasn’t the case.

On February 23, 2020, researchers from China, France and the U.S. released a joint analysis of more than 450 COVID transmission events in 93 cities in China. The analysis focused on the serial interval: the time between when someone exhibits symptoms and when the person they infect exhibits symptoms. Counter to expectations, the analysis showed that COVID’s serial intervals were often less than zero, meaning individuals exhibited symptoms before the person that infected them. These statistics were evidence of rampant presymptomatic transmission. Public health experts tried to raise the alarm that efforts to stop transmission via symptom screening (e.g., testing for elevated temperature or shortness of breath) were bound to fail and that “unprecedented measures” were needed to fight back.

The deadly consequences of asymptomatic transmission soon arrived in the U.S. On March 10, 2020, the Skagit Valley Chorale gathered outside Seattle for a rehearsal. Despite efforts to limit physical contact, within a few days it was evident that someone in the group had unwittingly infected others. Ultimately, 53 of the 61 attendees were infected, and two died. This superspreading event revealed that COVID could spread in the air in the absence of symptoms. Yet the relevance of asymptomatic transmission remained contested. On June 8, 2020, a top WHO official declared that asymptomatic transmission was “very rare.” The pandemic was raging, but we were losing precious time to confront silent spread. The consequences were grave. As head of the White House Coronavirus Task Force, Anthony Fauci noted in August 2020: “I’ve never seen a viral disease in which you have such a wide breadth of symptoms, ranging from no symptoms at all, in 40–45 percent of cases, to severe enough to kill you.” Asymptomatic transmission represents a double-edged sword. Individual outcomes may be better, but silent spread leads to many more infections that can lead to worse outcomes for the population.

What can be done to reduce asymptomatic transmission? Initial responses to the pandemic involved limitations on gatherings and stay-at-home orders. But COVID’s unusual mix of severe and asymptomatic outcomes catalyzed a diverse group of stakeholders to invest in unconventional approaches to reduce the risk of silent spread. These approaches include real-time risk assessment, large-scale rapid testing, context-specific masking and improved indoor air quality. Each of these has a complementary role in reducing silent spread, and if implemented at scale, they can be essential weapons in the ongoing fight against pathogens of pandemic potential.

In the absence of symptoms, real-time risk assessment powered by outbreak models and disseminated via mobile-accessible dashboards could function as a threat forecast. These dashboards could provide mapped information on a variety of infectious disease risks, including upsurges of COVID reported in wastewater. People could then decide to avoid events whose risk exceeded their tolerance. However, even if someone attends an event, the use of on-site rapid testing and masks could limit infections. This could be an enormous force for good, especially in nursing homes and long-term care facilities, which had a disproportionately large fraction of overall COVID fatalities. Irrespective of individual action-taking, infrastructure investments in indoor air quality (via improved filtering, air turnover rates and upper room UV-C sterilization) could improve health outcomes.

Finally, we must commit significant resources to the development and effective dissemination of vaccines both in the U.S. and globally—especially in developing countries. The production of billions of doses of vaccines just a year after COVID’s emergence represents an incredible validation of the power of basic research and public-private partnerships. However, producing vaccines does not always translate to getting shots into arms. Public health agencies must improve messaging to explain both why individuals can benefit from vaccines, when they should get vaccines (and boosters) and what each vaccine is meant to do. In the case of COVID, mRNA vaccines were shown to reduce rates of symptomatic illness by more than 90 percent. Yet these vaccines do not prevent all infections. This means vaccinated individuals can still get infected, test positive and infect others—but their risk of severe outcomes decreases. This is precisely the point. But the fact that vaccines did not provide perfect protection against infection (asymptomatic or otherwise) has accelerated the rampant spread of misinformation that threatens to diminish vaccine uptake—not just for influenza and COVID but also for preventable childhood diseases, including measles.

Nearly five years have elapsed since early warning signs emerged of a novel coronavirus spreading in Wuhan fueled by asymptomatic transmission that would soon lead to a global pandemic. At the time, the risk to public health and socioeconomic stability seemed far removed. Since then scientists, public health experts, government agencies and the biotech sector have developed a suite of countermeasures to confront the dangers of silent spread—yet there is more to do, including identifying the consequences of the silent spread of avian influenza in wild and domestic animals. Translating this momentum into data-driven threat assessments, high-impact interventions (spanning testing and air quality improvements), faster vaccine deployments and more effective messaging from doctors and public health agencies is essential to reduce the ongoing burden of COVID; these actions will better prepare the world to identify, prevent and respond to threats of pandemics to come—before it is too late.

Resources

nationalgeographic.com, “COVID-19 can ruin your sleep in many different ways—here’s why.” By Emily Sohn; nationalgeographic.com, “COVID-19 can interfere with your period in many ways. Here’s how.” By Meryl Davids Landau; nationalgeographic.com, “Why does COVID-19 cause brain fog? Scientists may finally have an answer.” By Sanjay Mishra; scientificamerican.com, “We Indulged Our Child During COVID Lockdown. Did That Change Him?” By Michael Venutolo-Mantovani; scientificamerican.com, “COVID Rates Are Rising Again. Why Does It Spread So Well in the Summer?” By Tanya Lewis; natiionalgeographic.com, “What is POTS? This strange disorder has doubled since the pandemic.” By Rachel Fairbank; scientificamerican.com, “Long COVID Is Harming Too Many Kids.” By Blake Murdoch; theepochtimes.com, “Jury: Bay Area Transit Workers Fired for Refusing COVID-19 Vaccine to Get More Than $1 Million Each.” By Jack Phillips; scientificamerican.com, “Confronting the Dangers of Silent Spread Is Necessary to Prevent Future Pandemics.” By Joshua S. Weitz;

How sleep and the immune system affect each other

Why sleep problems continue after COVID infection

A direct link from insomnia to respiratory illness

Developing drugs for COVID-related sleep disorders?

The impact of psychological stress

How to improve sleep after COVID-19

Poor messaging

Both virus and vaccine may temporarily alter menstruation

How does coronavirus change a period?

Vaccines trigger more minor shifts

Pruning connections between neurons is essential for learning

Using brain organoids to study neural damage

Is the loss of synapses causing brain shrinkage?

Exercise and POTS

When exercise backfires

Fitting their own needs

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