Pat Hartman | Childhood Obesity News

Coronavirus Chronicles — Transmission and the Pandemic

Pat Hartman June 22, 2020 1 Comment

“Denial ain’t just a river in Egypt.” Although that maxim is frequently heard in 12-step groups, Mark Twain is credited with saying it first.

Well, transmission ain’t just the gearbox in a car. It’s how the disease spreads from person to person, and relatively little is known about that subject. At first, the world thought children were relatively safe from either catching or passing along COVID-19. As more information became available these beliefs, like many others, began to wilt. Science connected the dots between obesity and race… and then between obesity and the virus.

When it comes to figuring out transmission, the trouble is, we don’t have enough dots.

Damned if you do, damned if you don’t

The public wants definitive information on how to protect itself from the threat. It does not want to wait for more reliable science. It wants to know everything, and reach its own conclusions. The public clamors for the facts. Researchers and the press oblige, with detailed information about how long the virus can live on various surfaces in the home and workplace, and what chemicals to clean surfaces with, and how often.

Science moves on, and wider research brings new facts to light. Then after a while, the experts announce, “Maybe we don’t have to worry so much about surfaces.” The public feels betrayed. But it hopefully grasps the next news story anyway. Then, there is another letdown. A promising lead fails to pan out, and the irate public demands, “Then why did you tell us that other thing? Don’t you even know what you’re doing? We’re getting you fired.”

When new information arrives, a certain segment of the public believes that the cover is now being stripped away from deliberate lies. Sometimes, the wackiest conspiracy theories turn out to be not so theoretical, and that obfuscates things even more.

Two steps forward, one step back

There was a widely publicized misunderstanding over hidden carriers, silent spreaders, superspreaders, asymptomatic people, pre-symptomatic people, and so on. Team of writers from the platform Medium.com expanded on that subject. Among others authorities, they contacted Harvard’s Jeremy Faust, M.D., who said,

The message should have been that symptom-free spread has been difficult to detect via contact tracing, not that it isn’t happening.

One problem is that “asymptomatic” is a very misleading term. Journalist Markham Heid quoted Eric Topol, M.D., of the Scripps Research Institute, and provided context:

Just because someone is asymptomatic does not mean that the virus is not doing damage.“If you do a CAT scan of these patients’ lungs, you see significant abnormalities tied to Covid, and these are woefully understudied,” [Dr. Topol] says. “We also know this the virus can go to the heart and kidneys, so that needs to be looked at too.” It’s possible, he adds, that these “below-the-surface problems” may increase a person’s risk for long-term health complications, such as the eventual development of lung disease.

The very nature of the disease is uncertain. The science establishment has been thinking of it as respiratory, but it might be vasculotropic. Maybe we should not even be looking at antiviral drugs, but concentrating instead on statins and ACE inhibitors. It isn’t a “po-tay-to/po-tah-to” kind of debate. As it turns out, to label something as a circulatory system illness rather than a respiratory illness has widely different implications. Lungs are lungs. But blood vessels are in every nook and cranny of the body — 60,000 miles of them.

(More on transmission next time…)

Your responses and feedback are welcome!

Source: “What the WHO Really Meant Regarding Asymptomatic Spread,” Medium.com, 06/09/20
Source: “What You Need to Know About Asymptomatic Spread of Covid-19,” Medium.com, 06/10/20
Image by Bryan Alexander/C BY 2.0

Coronavirus Chronicles — Three Factors and a Virus

Pat Hartman June 19, 2020 No Comments

Despite a national death toll of almost 120,000, and somewhere north of 10,000 new cases since yesterday, large segments of America currently seem willing to pretend that COVID-19 does not exist. Today’s post gathers up a few more instances of the multiple intersections between obesity, poverty, and race.

Those three factors also interact with COVID-19, to their detriment. A quotation from Commentary senior writer Christine Rosen includes both a rebuke and a warning:

There’s a great deal we don’t know about how COVID kills, but we do know a lot about obesity and its associated health risks. Educating the public about those risks isn’t racist, or fat-phobic, or any other intersectional indictment that activists can conjure. Like washing one’s hands and wearing a mask during a pandemic, it’s simply good public health policy.

Why does the public need to be educated? Here is a small example, from a recent article giving advice on how to (psychologically, emotionally) survive the whole family staying home together. The writer suggests a nostalgic return to the days of playing soccer in front yard. Or hitting baseballs.

Say what?

That particular writer may possess a deep sociological consciousness. No informational prose can indulge every possible caveat, exception, or equivocation that might occur to a writer. Still, it has to be sadly admitted that quite a few Americans would not pause for a second to question the assumption that everybody lives in a house with a front yard. Millions of us do not live in houses. Many times, there is no grass out front, but cement slabs or some unfriendly surface.

Even among the prosperous (relatively) few who own or rent homes with front lawns, how many of them are far enough from the street to be safe? How many can afford to be cavalier about the possibility of a baseball shattering a neighbor’s window; or of a soccer ball rolling into the street followed by a child… followed by an inattentive driver, and an ambulance? That also brings up the difficulty of maintaining equipment. Soccer balls get run over. Sometimes they get stolen. There are Americans whose day-to-day reality does not include buying sports equipment.

Decisions

Of course, all potentially helpful suggestions need to be set on the table. Goodness knows, Childhood Obesity News has offered hundreds of them to our visitors. But parts of the public harbor misconceptions about other parts of the public, and that is not helpful. Those of us who are fortunate, prosperous, and privileged — and even those who are marginally getting by — must not be left unaware of how many Americans are operating at bare survival level, or of the obstacles they often face.

The government, and various helping agencies, need to bear in mind that no matter how excellent the suggestions are, some of us don’t have the geographical opportunity of front-yard soccer. Some grownups can’t even manage to get to a store, because they don’t have anyone to leave their children with.

Limitations are one of the subjects covered by professor of sociology Sabrina Springs, who mentions such historical injustices as “the legacy of redlining that pushed black people into poor, densely populated communities.”

(To be continued…)

Your responses and feedback are welcome!

Source: “Where Do Obesity and Racism Really Collide?,” CommentaryMagazine.com, 05/27/20
Source: “It’s Not Obesity, It’s Slavery,” NYTimes.com, 05/25/20
Image by muffinn/CC BY 2.0

Coronavirus Chronicles — Obesity, Poverty, Race

Pat Hartman June 18, 2020 2 Comments

The disease itself is bad enough, but coronavirus has the distinction of being particularly exacerbated by the heavy additional burdens of race and racism. As we have seen, America’s minority groups are coincidentally affected by genetic factors that predispose many individuals to become obese, and obesity is the most widely-shared risk factor for COVID-19. On top of that, the societal forces that shape the lives of minority group members bring in an additional slate of risk factors.

Of course there is not a 100% correlation between ethnic heritage and poverty in the United States. Obese and economically disadvantaged white people are also in a world of hurt. Prosperous black and brown people are relatively protected from both the likelihood of contracting the virus, and from its consequences. Those realities are solid. But today, our topic is the intersections between obesity, poverty, and race — and, of course, the virus.

Dr. Andrew G. Rundle and others have spoken rather definitively on the subject:

What is very apparent from the data is that kids experience unhealthy weight gain during the summer, that it’s more so for African-American and Hispanic kids, and that the weight gain that occurs during the summer does not get worked off during the school year.

At the best of times, poor and/or minority kids don’t have the advantage of sports camps and other strenuous, calorie-burning summer options. This year, it’s more difficult than ever to send them off to a shared-custody parent or other relative, who might live in a more physically challenging environment. If they are already overweight, they are spending the summer in the same place where they became overweight.

Across every economic class, they are probably bingeing on screen-time of various sorts, and also on whatever food they can get their hands on. If food is available at all, parents are likely to be extra-lenient about distributing it, for a variety of psychological reasons.

Michelle Obama had a dream

In the 1970s, writes Christine Rosen, America’s childhood obesity rate was 5%. (Today’s number is almost quadruple — 18.5%). In her role as First Lady, Michelle Obama sought to turn back the clock and return to 5%. The preferred timeline would have that happen by 2030, which is 10 years from now. Quite frankly, it does not appear likely. Rosen says,

Those most at risk? Black and Hispanic children. In an address to the NAACP in 2010, the First Lady was pointed about the urgent need to improve children’s health in communities of color.

Currently, many authors are preparing or defending works that offer reasons for the disparity.
Sociologist Sabrina Springs vehemently opposes the idea that African Americans are noticeably disadvantaged in this area, especially by obesity. She says,

The cultural narrative that black people’s weight is a harbinger of disease and death has long served as a dangerous distraction from the real sources of inequality.

But Rosen returns to the theme:

Obesity has measurable, significant effects on people’s health. Four out of five African-American women are overweight or obese… [T]he causes are “multi-factorial,” including genetics, socioeconomic status, and environment. Individuals’ own poor food choices also play a rule.

(To be continued…)

Your responses and feedback are welcome!

Source:”Endless Summer Puts Homebound Kids at Risk for Weight Gain,” NYTimes.com, 04/30/20
Source: “Where Do Obesity and Racism Really Collide?,” CommenraryMagazine.com, 05/27/20
Image by Pat Hartman

Coronavirus Chronicles — Three Plagues

Pat Hartman June 17, 2020 No Comments

In America, racial issues have been present for centuries. The intensity of the conflict waxes and wanes, but it is always present in some degree. In the past few weeks, thanks to the deplorable actions of some backward-looking and seriously malicious individuals and groups, race consciousness and animosity have spiked.

Obesity, on the other hand, does not have a jagged up-and-down graph, it just continues to go up and up. Also, defying our preference to ignore or forget COVID-19, it is still around, casting its ugly shadow on every aspect of our lives. Despite loose talk of an impending “second wave,” it is clear that the country is still in the midst of the first wave. Sheer desperate denial does nothing to improve any of these realities, and they have teamed up in an increasingly threatening partnership.

Born into risk

African Americans, Latinx Americans, Pacific Islanders, and some other minority groups have very unfortunate genetic foundations on which to build their health houses. They are prone to obesity and endangered by all the co-morbidities that come along with obesity. Black and (to a lesser extent) Hispanic Americans are more apt to become victims of the virus. Lockdowns are undertaken for the public safety, to decrease the spread of the virus, but the enforced immobility encourages obesity to flourish.

And to complete the circle of hellish consequence, obese people have a worse experience with the illness. Against minority-group Americans, obesity and COVID-19 work like tag-team wrestlers. Journalist Maitefa Angaza covers the many contributing societal factors — income inequality, disparities in levels of health care, racism, and now a pandemic disease — and a heritage of obesity that causes, or worsens, hypertension, diabetes, cardiovascular disease, stroke, and even some cancers.

Of course obesity is, to a certain extent, a modifiable risk factor. But as Angaza remarks, “When the stress piles on, most people tend to overeat.” She elaborates on the theme:

Childhood obesity is at record levels, with Black students about 65 percent more likely to be obese than white students… Weight control can no longer be seen as an avoidable nuisance; COVID-19 has made that clear. Obesity often makes the difference between those who survive the coronavirus and those who succumb, because the severity of the virus’ impact is heightened by obesity’s pre-existing illnesses.

It is no different in Great Britain, where the acronym BAME stands for “black, Asian, and minority ethnic.” For ContemporaryHealth.co, Nicholas Feenie notes that even in the midst of tons of intimidating statistics, “perhaps the most shocking are the numbers of people from black, Asian and minority ethnic backgrounds who have died from Covid-19.”

This includes doctors and other health care professionals from those vulnerable ethnic groups, who are among the first to succumb to the contagion, and disproportionately likely to die from it. Between the fatality rates of people from these backgrounds and white people, the disparities are blatant and shocking.

Just a few days ago, when the American death toll had reached 112,000, APM Research Lab published some alarming American statistics, expressed in several different ways:

Collectively, Black Americans represent 12.4% of the population in the U.S., but they have suffered 24.3% of known COVID-19 deaths — i.e., they are dying at twice their population share.

White Americans represent 62.2% of the population in the U.S., but they have experienced 51.7% of deaths.

Collectively, Indigenous, Asian and Latino Americans are dying roughly proportional to their population share.

1 in 1,625 Black Americans has died (or 61.6 deaths per 100,000)
1 in 2,775 Indigenous Americans has died (or 36.0 deaths per 100,000)
1 in 3,550 Latino Americans has died (or 28.2 deaths per 100,000)
1 in 3,800 Asian Americans has died (or 26.3 deaths per 100,000)
1 in 3,800 White Americans has died (or 26.2 deaths per 100,000)

Your responses and feedback are welcome!

Source: “The Black Obesity Epidemic and Coronavirus,” OurTimePress.com, May 2020
Source: “Covid-19, Obesity, BAME… and Vitamin D,” ContemporaryHealth.co, 05/06/20
Source: “The Color of Coronavirus,” APMResearchLab.org, 06/10/20
Image by muffinn/CC BY 2.0

Coronavirus Chronicles — Life Comes At You Fast

Pat Hartman June 16, 2020 1 Comment

Dr. Michael Osterholm directs the Center for Infectious Diseases Research and Policy at the University of Minnesota. About a month ago, in an interview he said that COVID-19 is very complicated, and “The more we learn about it, the more we realize how little we know about it.” He emphasizes the crucial importance of quickly identifying individuals who have it, so they can be isolated.

But people pass this thing on to others before they even know they have it themselves, and sometimes they never know, because they never feel sick. Journalist Sara Chodosh wrote,

Some early models suggested up to 55 percent of the disease’s spread could be due to these hidden carriers, which make up an unusually high number of the virus’s total cases. A large testing mission in San Francisco found that around 50 percent of people with COVID-19 had no symptoms.

The Centers for Disease Control posited that 40% of transmission occurs before transmitter even feels bad. We were starting to hope we had a handle on the basic principles of contagion logistics. Then, a flareup of crossed signals emanated from the World Health Organization, which held that such transmission is rare, a statement that was then extensively unpacked, walked back, spun, and several other past-tense verbs based in public relations terminology.

One of the statements seemed to assert that the definition of “symptom” had been narrowed down to “droplets.” But some people shed virus like crazy, and never even spike a temperature. It was all very confusing.

A group of authors from the publishing platform Medium put together an explainer from which these sentences are excerpted:

It’s important to note that asymptomatic people who never exhibit signs of Covid-19 are different from pre-symptomatic people who initially don’t have symptoms but develop them later. It’s difficult, from a research standpoint, to tease these two groups apart.

The real conundrum is pre-symptomatic transmission… People appear to have the highest number of viral particles in their body, called the viral load, at the beginning of an infection right before they develop symptoms. Experts think people are most infectious when their viral load is highest…

This means a cough isn’t required to expel SARS-CoV-2 viral particles — just breathing or speaking could be enough, particularly when someone is shouting, singing, or breathing heavily from exercise.

Driving the point home, the authors emphasize again that there is “no simple way to distinguish between asymptomatic people and pre-symptomatic people when they are out in the world…” Pre-symptomatic people might be at large for as long as two weeks without anyone having a clue. Many businesses and institutions depend on hand-held thermometer guns, and perhaps they should not.

Some critics deprecate all this pursuit of what seems to some more of an etymological debate. But petty as it might appear, all this is of monumental importance. Words definitely need to be quibbled over. Everybody needs to know what everybody else is talking about. Before we send kids back to school we need to know what’s what, in no uncertain terms. We all need to be, as the saying goes, on the same page.

Which brings us back to the extremely uncomfortable reality revealed by Dr. Osterholm: “The more we learn about it, the more we realize how little we know about it.”

Your responses and feedback are welcome!

Source: “Transcript: Dr. Michael Osterholm speaks with Michael Morell on ‘Intelligence Matters’,” CBSNews.com, 05/13/20
Source: “The truth about asymptomatic COVID-19,” PopSci.com, 06/09/20
Source: “Coronavirus spread by asymptomatic people ‘appears to be rare,’ WHO official says,” CNN.com, 06/09/20
Source: “What the WHO Really Meant Regarding Asymptomatic Spread,” Medium.com, 06/09/20
Image by muffinn/CC BY 2.0

Coronavirus Chronicles — If We Only Knew

Pat Hartman June 15, 2020 No Comments

Science is often a “two steps forward, one step back” sort of process. Discoveries turn out to be not quite what they originally seemed. Answers transmogrify back into questions. Childhood Obesity News described one of the ideas about how COVID-19 affects some victims, by triggering a cytokine storm, in which extreme inflammation takes place in the whole body because of immune system overreaction. Cytokines are good in moderation, but too many of them can cause multiple organ failure and death.

In the case of an obese patient, a connection is hypothesized with the inflammation that is already present because of the actions of fat cells. Complications like blood clots, heart problems, and neurological symptoms seemed to fit with this theory too, because they have been known to occur in other respiratory illnesses.

Related mysteries

For The New York Times, Pulitzer Prize-winning reporter Pam Belluck described
Multi-system Inflammatory Syndrome in Children, or MIS-C (also known as Pediatric Multi-system Inflammatory Syndrome), which…

[…] has shaken widespread confidence that children were largely spared from the pandemic. Instead of targeting lungs as the primary coronavirus infection does, it causes inflammation throughout the body and can cripple the heart. The syndrome often appears weeks after infection in children who did not experience first-phase coronavirus symptoms.

Meanwhile, medical professionals have been disappointed by their inability to save numerous patients even with ventilators. By means of those highly-regarded and very costly machines, air is unequivocally introduced into the lungs. So, what’s the problem? Journalist Dana G. Smith, who covers health, science, and wellness, describes it:

Moving air into the lungs, which ventilators help with, is only one part of the equation. The exchange of oxygen and carbon dioxide in the blood is just as important to provide the rest of the body with oxygen, and that process relies on functioning blood vessels in the lungs.

Coronavirus seems determined to defy any attempts at pattern recognition that could help defeat it, and experts have more than once used the word “bizarre” to describe its habits and effects. There is a need for a Unified Field Theory of COVID-19. Smith traces the various bits of information that scientists are piecing together in an attempt to figure out such questions as why some children don’t even get symptoms, while others get heart attacks.

For a clear explanation, the writer interviewed Mandeep Mehra, M.D., medical director of the Heart and Vascular Center at Brigham and Women’s Hospital in Boston, and published an article titled “Coronavirus May Be a Blood Vessel Disease, Which Explains Everything.” Without providing all the spoilers, we will say here that it contains such terminology as endothelial dysfunction, vasculotropic virus, ACE inhibitors, plaque rupture, and myocardial infarction.

Your responses and feedback are welcome!

Source: “‘Straight-Up Fire’ in His Veins: Teen Battles New Covid Syndrome,” NYTimes.com, 05/17/20
Source: “Coronavirus May Be a Blood Vessel Disease, Which Explains Everything,” Medium.com, 05/28/20
Image by muffinn/CC BY 2.0

Coronavirus Chronicles — Superemitters, Good Atomizers, Silent Spreaders, and Superspreaders

Pat Hartman June 12, 2020 2 Comments

Superemitters and good atomizers are people whose bodies for some reason go above and beyond the call of duty, in terms of pushing viruses out into the world. People who experience cold winters have watched clouds of water vapor issue from others’ mouths, in the phenomenon known as “seeing your breath.”

In the picture on this page, the fellow has nicotine and other chemicals coming out of him, but imagine that instead, the particles are millions of invitations to the worst experience of your life, a case of the COVID-19. How close to this person would you want to stand? Wouldn’t it be great if one or both of you wore a face covering?

Science used to believe that when someone coughs or sneezes most of the germs land within a foot and a half of the expulsion point. For NewYorker.com, Atul Gawande described a study conducted in the 1940s:

[O]ne recruit spewed large quantities of bacteria into petri dishes and air samplers almost ten feet away. “This subject,” the report noted, “was really an unusually good atomizer.”

It has now become well recognized that, under the right conditions of temperature, humidity, and air circulation, forceful coughing or sneezing can propel a cloudburst of respiratory droplets more than twenty feet.

A good atomizer can be a superspreader. By now, the lore of the coronavirus is filled with stories of superspreader events. Sadly, many of them are sponsored by churches. There’s the choir practice where one very infectious woman got dozens of people sick. In his article for Medium.com, health and science journalist Robert Roy Britt explains,

People with the coronavirus can be infectious two to three days before symptoms start, during a period called incubation. Some carriers, particularly younger people, may spread the disease and never have any symptoms. These people, a subset of superspreaders, are called “silent spreaders.”

What about kids? The odds of a child (especially if not obese) getting the disease are slight. But when they do, the results can be horrible.

Or they might have no symptoms of illness at all, and function as extremely efficient little superspreaders. Parents of small children are full of stories about the germs their kids bring home from preschool. Affectionate children tend to hug. Kids are not always conscientious about keeping their secretions to themselves.

Gawande wrote, “At the right point in the illness, under the right environmental and social conditions, one person can produce a disaster.” Can that person be a child?

Your responses and feedback are welcome!

Source: “Amid the Coronavirus Crisis, a Regimen for Reëntry,” NewYorker.com, 05/13/20
Source: “The Science of Superspreaders,” Medium.com, 06/04/20
Image by www.vapes.com/(CC BY 2.0)

Coronavirus Chronicles — “Super” Just Means “Above”

Pat Hartman June 11, 2020 1 Comment

Above, over, or beyond — that is what “super” means in its native tongue, Latin. No judgment is involved. A thing can be super good or super bad. Used as a prefix, super is a standard of medical lingo, and the COVID-19 epidemic has provided several opportunities for it to be used. For instance, what is a superspreader? First, we need to know the normal rates of transmission for any communicable disease.

For The New Yorker, Atul Gawande explained the meaning of the reproductive ratio, or R0 (pronounced r-naught, which means zero), using the familiar disease of measles. At a school where 30% of the students had not been vaccinated, “each infected child spread the virus to, on average, eighteen others.” So the R0 was 18. Here is where it gets scary:

By comparison, a person with covid-19 will infect, on average, only two to three others… But an R0 of two or three is more than enough to cause a pandemic. [A] single unchecked case can lead, over two months, to more than twenty thousand infections and a hundred deaths.

If that sounds extreme, think back. Have you ever known a person with badly-fitting dentures and, when the lighting was just right, understood how much they sprayed? Robert Roy Britt wrote,

The number of respiratory particles sprayed out while talking, most of them not noticeable to the human eye, can range from one to 50 per second, depending largely on how loud a person talks… But some “superemitters,” for mysterious reasons, emit 10 times more than others while conversing…

This is useful to bear in mind when thinking about the importance of face coverings. Regarding contagion events that happened just three months ago, Britt reports on a fateful Bible study group attended by 92 people, including a man who had contracted COVID-19, but not yet developed any symptoms. Then 35 people caught it from him, and 26 people in the larger community caught it from them.

The sponsors of a cruise to Antarctica took the temperatures of more than 2,000 passengers before they embarked on the journey. The sly coronavirus slipped in anyway, and 59% of the passengers had it. Since the R0 of the disease has seemed to be so relatively low, these massive infections seem statistically unlikely.

But apparently, one exceptional person can affect dozens or hundreds of others. Some experts believe that 80% of the COVID-19 cases are instigated by 20% (or maybe even just 10%) of infectious individuals, who are known as “superspreaders.”

You can’t always leave the kids at home

The nature of the event matters, too. If it involves shouting or singing, like a church service, the danger increases. If it involves crowds and toxic gases, like a demonstration attacked by police, the danger increases a lot.

Tear gas has triggered choking, bronchitis, blistering, and lingering lung damage. People with hypertension, emphysema, or coronary artery disease can be very severely affected. One gas used is 2-chlorobenzylidenemalononitrile, or CS for short. It can cause the lungs to swell and bleed.

For Forbes.com, Judy Stone wrote:

CS does much of its nasty work by binding to a pain receptor named TRPA1, located all over our bodies — in our respiratory, GI tracts and skin. CS entering buildings contaminates furniture […] resulting in prolonged contact and irritation. Children, with developing lungs and immune systems, are at special risk…

Stone notes that tear gas and pepper spray both increase the susceptibility of humans to COVID-19. She goes on to say,

The chemicals destroy tissue, making them more susceptible to infection. Also, if someone already has an infection, the violent coughing that is caused by these noxious agents will undoubtedly cause them to spew secretions and may well cause super spreading events…

In an ideal world, there would not be many children on a cruise ship or in a protest crowd. But of course kids come in contact with adults who might be.

(To be continued…)

Your responses and feedback are welcome!

Source: “Amid the Coronavirus Crisis, a Regimen for Reentry,” NewYorker.com, 05/13/20
Source: “The Science of Superspreaders,” Medium.com, 06/04/20
Source: “Tear Gas And Pepper Spray Can Maim, Kill And Spread Coronavirus,” Forbes.com, 06/08/20
Image by Ben/CC BY-SA 2.0

Coronavirus Chronicles — MIS-C or PMIS? Two Names, One Mystery

Pat Hartman June 10, 2020 1 Comment

Every day, reports continue to come out about COVID-19. Some confirm previous beliefs, and others add new knowledge. It now seems very, and dishearteningly, clear that people are flagrantly contagious before they show any symptoms (if indeed they ever do). While some people never even realize they are afflicted with an illness, others feel bad for a really long time.

There are sub-categories of victims with their own special problems and needs. A very recent study from a children’s hospital in New York made four generalizations about pediatric patients:

Children hospitalized with COVID-19 commonly had comorbidities, infants had less severe disease, those with obesity were likely to receive mechanical ventilation, and elevated markers of inflammation at admission and during hospitalization were associated with severe disease.

It became clear pretty early on that obese children are more likely to contract the illness and to have a more difficult time; and that children from America’s black and Hispanic minority groups, with a greater susceptibility to the disease in the first place, are likely to have the most miserable experience of all. But wait, it gets even worse.

Inflammation can go right off the charts into a territory known as Multisystem-Inflammatory Syndrome in Children, or MIS-C, a rare and miserable condition that doctors don’t even know what to think about. They have not even agreed on a name for it yet, with some calling it Pediatric Multi-system Inflammatory Syndrome, or PMIS.

But what is MIS-C or PMIS?

Is it just part of a very bad case of COVID-19, or a separate yet related entity that sets in after the acute viral stage is over? Why the doubt? Because, maddeningly, most of the kids who have it do not even test positive for the coronavirus. Yet they have the antibodies that indicate recovery from it. (Another question: Why do there seem to be no cases of it in China, or even on the West Coast of the U.S.?)

According to one theory, a child might have developed antibodies during an active case that she or he recovered from the first time around, without even appearing sick. But with additional exposure to the virus, which is still quite present in the community, the body gets exasperated and says, “Hey, I thought we did this already,” and throws up a really emphatic defense that ends up wreaking more damage than the disease itself.

Untreated, MIS-C can do ridiculous things like give a six-year-old a heart attack. Yet despite its severe nature, doctors are said to be reluctant to name that diagnosis because the treatment for it is very rough on tender young humans. And no matter what course the rampant inflammation takes, the long-term outlook for the recovered child is not good.

Parents must remain obsessively, intrusively, annoyingly vigilant. One unsavory possibility is that, reluctant to face another hospital admission, the child might hide any health detail that would betray a recurrence of MIS-C.

Your responses and feedback are welcome!

Source: “Epidemiology, Clinical Features, and Disease Severity in Patients With Coronavirus Disease 2019 (COVID-19) in a Children’s Hospital in New York City, New York,” JAMANetwork.com, 06/03/20
Source: “Doctors Race For Answers As Kids Fight Rare Inflammatory Syndrome Tied To Coronavirus,” NPR.org, 06/07/20
Image by Iforce/Flickr

Coronavirus Chronicles — If Only We Had Listened

Pat Hartman June 9, 2020 1 Comment

The uncanny and unwelcome affinity shared by fat cells and the COVID-19 organism was the subject of the most recent post. For the more imaginative among us, this Coronavirus era might seem like an episode in a long-running series called “If Only We Had Listened.”

If only the Let’s Move! initiative had been adopted and fully implemented in every corner of America, would there be fewer obese adults today? Yes. Would there be fewer obese children today? Also, yes.

Would institutions and governments be paying such huge amounts to treat the virus and its co-morbidities? No, they would not. Would neighborhoods have strengthened their exercise potentialities? Very possibly. Would more families have at-home exercise options at the ready? Quite probably.

If only we has listened to Michelle Obama, would quite the same number of humans be suffering right now from either obesity or coronavirus, or both? No.

What is the problem again?

Obesity exacerbates the virus, and at the same time, the virus worsens the obesity. Fat in the upper abdomen squeezes the diaphragm and lungs, and prevents optimal breathing. And that’s bad enough. But mainly, the immune system goes into overdrive.

Writing for the UK-based College of Contemporary Health blog, Nicholas Feenie notes,

In individuals with obesity, visceral adipose tissue in the abdominal cavity produces inflammatory cytokines that cause a chronic low-grade inflammatory state throughout the body… [O]ne theory is that inflammation caused by obesity occupies the immune system’s resources, reducing its ability to mount an effective response against the virus.

On the other hand, it has also been proposed that this constant activation of the immune system means that it overreacts to the virus, causing excess inflammation and damage in the lungs.

A few days ago, news came out of a case series concerning 50 hospitalized pediatric COVID-19 patients. Many, but not all, had respiratory symptoms. Some of the kids had bad cases, and their inflammatory markers were high. Among their numbers, neither infants nor the immunocompromised were worse off. But the obese children in the cohort were more likely to have severe cases.

More factors

Statisticians, of course, make predictions. For MedicalDaily.com, Darwin Malicdem did a thought experiment about the school closures in the United Stated continuing for the rest of the year 2020, which is not even half over yet. He says that could very well mean a 2.4% increase in childhood obesity by then, and a total of well over a million new childhood obesity cases by next March. This would be nobody’s idea of a good time.

Your responses and feedback are welcome!

Source: “Covid-19 and Obesity,” ContemporaryHealth.co.uk, 04/30/20
Source: “Epidemiology, Clinical Features, and Disease Severity in Patients With Coronavirus Disease 2019 (COVID-19) in a Children’s Hospital in New York City, New York,” JAMANetwork.com, 06/03/20
Source: “More Kids At Risk Of Obesity In US Amid COVID-19 Pandemic,” MedicalDaily.com, 06/01/20
Image by muffinn/CC BY 2.0

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