Coronavirus news & views

Vaccinating Pregnant Women And Kids Against COVID: Suspicion vs Science

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“There are in fact two things, science and opinion; the former begets knowledge, the latter ignorance.”

-Hippocrates

Background. The announcement in May on X by Health Secretary RFK, Jr. that the CDC will no longer recommend COVID vaccinations for children over 6 months and pregnant women took the entire CDC by surprise. Kennedy’s decree represents a profound policy shift as well as a major assault on science-based medicine. It completely abandons established procedures for vaccine policy development. Normally, recommendations for vaccines are made by the CDC director based on votes by the National Center for Immunization and Respiratory Diseases (NCIRD), and the Advisory Committee on Immunization Practices (ACIP), which meet in public with independent experts who review the evidence for vaccine safety and efficacy in order to make appropriate recommendations on their use. This review process was entirely bypassed. Kennedy made a solo decision without this sort of expert advice, public input, or peer review, which have long guided vaccine policy. This unvetted policy shift endangers vulnerable people, namely soon to be moms and their newborns who do not have a fully formed immune system, and young children. This surprise policy shift reflects Kennedy’s long-standing antipathy toward any vaccine. He is on record for claiming that there are no safe or effective vaccines. None.

Then, just days after Kennedy’s unilateral policy shift, the CDC came out with its own announcement that countermanded part of RFK, Jr’s. anti-vaccine mandate. The agency kept COVID shots on its schedule for kids 6 months to 17 years old, but did not change the vaccine denial for pregnant women even though the FDA has just cited pregnancy as a high-risk condition for severe COVID disease, and the CDC website continues to encourage pregnant women to get the vaccine. At this point, it is not clear which policy, Kennedy’s or the partial pushback policy from the CDC will rule.

Is Kennedy’s solo policy wise?

The evidence for vaccinating pregnant women. The scientific foundation supporting COVID-19 vaccination in pregnancy is overwhelming and unambiguous despite Kennedy’s notions. Consider the comprehensive systematic review of vaccinating over 17 million pregnant women, which found no safety concerns for COVID vaccination during pregnancy. Nada. This massive body of evidence, gathered across multiple countries and healthcare systems, demonstrates consistent COVID vax safety through all trimesters of pregnancy, with no increased risk for stillbirth, preterm birth, congenital malformations, or pre-eclampsia. This conclusion is further bolstered by numerous other studies, too. What is missing is any scientific evidence that the vaccine is dangerous for pregnant women or their fetuses. On the other hand, in contrast to the vaccine, COVID itself increases a pregnant woman’s chance for stillbirth, preterm birth, hospitalization, and death. This is because the pregnant woman is relatively immunosuppressed and more susceptible to various respiratory diseases including COVID. All countries, except the US now, believe that pregnancy is a risk factor for COVID. The American College of Obstetricians and Gynecologists (ACOG) agrees with the FDA that pregnancy is one of the significant risk factors for serious COVID outcomes. For this reason, they too strongly recommend that pregnant women receive a COVID vaccine.

Furthermore, maternal vaccination is doubly effective: it not only protects the mother from high-risk COVID complications, it also provides crucial protection over her newborn’s first six months via antibodies that are transferred from the mother to the fetus across the placenta. These antibodies from COVID-immunized women protect the newborn while it develops its own immune system so it can make its own antibodies. Specifically, ACOG released the following statement in response to Kennedy’s zealous policy manifesto:

“ACOG is concerned about and extremely disappointed by the announcement that HHS will no longer recommend COVID-19 vaccination during pregnancy. As ob-gyns who treat patients every day, we have seen firsthand how dangerous COVID-19 infection can be during pregnancy and for newborns who depend on maternal antibodies from the vaccine for protection. We also understand that despite the change in recommendations from HHS, the science has not changed. It is very clear that COVID-19 infection during pregnancy can be catastrophic and lead to major disability, and…. (t)he COVID-19 vaccine is safe during pregnancy, and…can protect our patients and their infants after birth.”

Thus, all the science shows that vaccination of pregnant women is a very good idea. Kennedy’s anti-science policy is not.

What about newborns who can’t be vaccinated because their immune systems are not developed? Kennedy’s policy change excluding soon-to-be mothers from vaccination creates an especially dangerous gap in protection for infants younger than 6 months old, who were previously protected by maternal vaccination during pregnancy. These babies, too young to be vaccinated themselves, relied entirely on antibodies transferred from vaccinated mothers for protection during their most vulnerable early months of life. By removing recommendations for maternal vaccination, the policy eliminates this critical shield for newborns who lack an immune system, leaving them exposed to a disease that can cause severe respiratory illness, multisystem inflammatory syndrome, and other serious complications. These newborns will have to wait until they develop their own immune systems in order to be able to fight off infections like that which causes COVID.

The evidence for vaccinating kids older than 6 months. Kennedy’s policy reversal against COVID vaccination in older children poses particularly grave risks for kids from the COVID complications described below.

The rational for not vaccinating kids is that since children are at less risk than seniors from significant COVID health problems, they don’t need vaccination against the CoV-2 virus, which causes the disease. However, data show that this benign notion is flawed. As of 2022, at least 1,800 children have died of COVID in the United States (that is the equivalent of six jumbo jet crashes). In other words, about 600 kids died each year from COVID, while the flu death rate in children only ranged from 39-199 per year since 2004. Thus COVID is much more lethal than influenza in children. Beyond these fully preventable COVID deaths, many more kids required hospitalization, including intensive care. In 2023, one million kids, or about 1.4% of children, came down with long COVID, the chronic problem that bedevils many COVID sufferers well after contracting the disease. In kids, long COVID problems include headache, fatigue, loss of IQ points, a variety of GI issues, and memory and other neurological problems. Neuroscience research has shown that young people who have recovered from COVID often show distinct changes in their brain activity as measured by scans while performing cognitive tasks.

Furthermore, kids can also develop a nasty multi-organ pathology known as Multisystem Inflammatory Syndrome, or MIS. MIS occurs post-infection and can lead to organ failure and other long-term health problems. The condition is reminiscent of toxic shock syndrome where different organs, including the heart, brain, lungs, kidneys, skin, eyes and GI system can become inflamed and/or fail. More than half of COVID MIS cases are under nine years old.

All together, these facts provide sobering reminders that this disease is not benign in pediatric populations. Vaccination protects kids against serious COVID disease and death as well as against these complications of long COVID and MIS.

 Despite these substantial problems kids can face from COVID, I keep encountering people who totally dismiss the disease in children simply because its effects are more devastating on older people with other co-morbidities. But, it really is a very poor reason to brush aside the effect of the disease in children simply because another demographic fares worse. It is even worse to use this argument to say that kids need not be vaccinated as Kennedy just did. In children, the mRNA vaccines are about 90% effective in preventing the disease and its complications, and this protection is durable. Other studies show that keeping kids up to date on COVID vaccines helps reduce illnesses, doctor visits, missed school, and complications from long COVID and MIS. Unvaccinated children were up to 20-times more likely to develop long COVID than those who were vaxed.

Bottom line. People who think that it is unnecessary to vaccinate pregnant women and young kids totally ignore well established science. As an immunology student, I remember learning some 50 years ago that maternal immunization provides important passive immunity for newborns from their mothers, giving babies time to develop their own immune systems. Furthermore, there is absolutely no credible evidence that such maternal vaccination harms the mother or the fetus. It also is abundantly clear that children over 6 months of age benefit in very important ways from COVID vaccination. Sure they seldom die from the virus, but all these deaths are preventable. Also, many more kids can and do succumb to serious complications from COVID that vaccination protects them from.

What rational person could be against protecting kids from a preventable disease?

New Data On COVID Vaccine Deaths

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“There are two ways to be fooled. One is to believe what isn’t true; the other is to refuse to believe what is true.”  - Soren Kierkegaard

Two years ago, a Kaiser Family Foundation poll showed that 34% of Americans believe that the COVID vaccines have caused thousands of sudden deaths. As a result, some health departments have been forbidden from promoting the shots or have had to even ban them. Furthermore, despite clinical evidence to the contrary, 27% of people believe that the vax itself causes infertility-it does not, and 31% still believe that the anti-parasite drug, ivermectin, effectively treats COVID-it has been proven not to.

The rumor of “thousands of deaths” was partly driven by viral videos of young, healthy athletes collapsing on the field, alleging COVID vaccines were to blame. One of the most promoted of the videos, Sudden Death, has been exposed in these pages and by others as fabricated and blatantly dishonest. In many of the examples shown in the video, it has been proven that the collapsing athletes hadn't received a COVID shot, and deaths that did occur happened well before COVID vaccines were even available! Absolutely no evidence for a vaccine-related death can be found in that video.

After the real on-field cardiac arrest of the Buffalo Bill's Damar Hamlin in 2023, another unsubstantiated rumor by Peter McCullough, an MD darling of the anti-vax crowd, reported that sudden deaths in athletes had increased dramatically after the vax rollout. But, an epidemiologist who dug into McCullough’s data, found that his numbers were inaccurate and inflated–for example, some of the "young athlete deaths" were not actually healthy athletes who died suddenly on the field, but instead were random news reports of people of all ages dying from many different causes, including an elderly woman who died at home! McCullough is now hyping a non-existing health problem in the US so he can sell people his nostrum he claims mitigates the problem. Go figure.

Cardiac arrest. In contrast to all this disinformation, a new study published in the Journal of the American Medical Association last February specifically looked into vaccine-associated deaths. It examined whether there was any increase in sudden cardiac arrest (SCA) (where the heart suddenly stops, but the person survives), or in sudden cardiac death (SCD) in young US athletes after either the appearance of COVID (2020) or the introduction of COVID vaccines in 2021.

The study found no association between the vaccine and cardiac problems. The highest year for both sudden cardiac arrest and death in the study was 2017, well before both the virus and vaccines were on the scene. Furthermore, the incidence of cardiac-related deaths did not change much from year to year, even AFTER the appearance of the virus or the vaccine! This is shown by the figure below (also notice how small the actual numbers are).

Astley et al, JAMA, 2025

This finding is further supported by other studies that also have shown no increase in cardiac arrest in young people in general (ages 5-50) during the COVID vaccine rollout in Australia, and an overall decreasing rate of rare sudden cardiac deaths in NCAA athletes during the COVID vaccine roll out in the US.

Myocarditis. Many conspiracy theories are rooted in partial truths that are overinflated and vaccine-induced myocarditis is no exception. There are real, but very rare, documented incidences of myocarditis (inflammation of the heart) after getting a COVID vaccine. Research from the Yale School of Medicine indicates that myocarditis happens in 0.036% of males age 12-17 after an mRNA vaccine. In contrast, this same age unvaccinated group experiences myocarditis twice that rate after COVID infection; thus the vaccine actually protects against the inflammation. Furthermore, vaccine-associated myocarditis is milder than other forms of myocarditis and patients quickly recover.

Bottom line. In reality, serious adverse events were very rare in large, randomized mRNA vaccine trials and occurred at a similar rate among people who got the vaccines and those who got the placebos. Finally, if the vaccines are so dangerous, why does the evidence proving that need to be fabricated?

Tracking The Origin Of Coronaviruses Via Viral Genome Sequence Analysis

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“You are welcome to my opinion.” 

-William F. Buckley

Background. In early 2020, during the first weeks of the COVID pandemic, an unsubstantiated rumor circulated (and is still around) that the CoV-2 virus that caused the pandemic was a biological weapon created by the Chinese Army. However, a group of scientists analyzed the genome sequence of the spanking new CoV-2 virus and rejected that idea saying there was no molecular evidence that the virus was man-made. Although they couldn’t rule out an accidental lab leak, they favored a natural origin of the CoV-2 virus at the time. Fast forward several years and the science still predominately favors the notion that the virus arose from a wild animal found at the Wuhan live market.

Eight of 18 US intelligence agencies have also examined the origin of the CoV-2 virus with mixed conclusions. Despite what scientists believe, the FBI, and more recently the CIA have come out in favor of an escape from the Wuhan Institute of Virology, although that conclusion is made with only the lowest of confidence. The Department of Energy intelligence folks also concluded with low confidence that the virus escaped from a different lab in Wuhan. Note that the intel community’s definition of low confidence intelligence is “that the information’s credibility and/or plausibility is uncertain, that the information is too fragmented or poorly corroborated to make solid analytical inferences, or that reliability of the sources is questionable.” Meanwhile, the remaining five intelligence agencies do not favor a lab origin scenario.

Importantly, the three agencies that favor a lab origin for the virus have not made their evidence public, so scientists cannot evaluate the bases for their conclusions. In contrast, several peer-reviewed science papers have been published on the topic and all conclude that the virus came from wild animals. Their prevailing understanding is that the virus then entered humans at the Huanan Seafood Market in Wuhan.

One of the most common arguments for the lab origin of CoV-2 is that the virus first infected humans in a city that was hundreds of miles away from where bat coronaviruses are endemic. Proponents of lab-leak theories have pointed to the long distance between Wuhan and the locations where the closest relatives of CoV-2 have been found as evidence for a lab leak. They believe that Wuhan is too far from where coronavirus-infected bats roamed for bats to be the source of human-infecting CoV-2. Furthermore, Wuhan has a coronavirus research lab (the Wuhan Institute of Virology or WIV). If Wuhan was too far for bats to fly and then infect wild mammals, some people assumed that scientists at the WIV must have developed the virus in a lab from which it either escaped or was released.

However, it is very relevant to note that in 2002 the first coronavirus, CoV-1, began infecting humans in Guangdong Province, China, which also was hundreds of miles from where bat coronaviruses are found. Notably, no lab in Guangdong Province studied coronaviruses. It was determined that a CoV-1-related coronavirus circulating in horseshoe bats jumped into raccoon dogs and other wild mammals in southwestern China. Some of those animals were caught and transported by humans for sale in markets in Guangdong where the coronavirus jumped again, into humans. The result was the first SARS pandemic, which spread to 33 countries and claimed 774 lives before non-pharmacological measure (read social isolation and masks) convinced it to quickly peter out in 2004 before any vaccine or medicine to treat it was developed. A few months into the first pandemic, scientists discovered the CoV-1 coronavirus that caused human disease (SARS) in mammals known as palm civets, which were sold in a market at the center of the outbreak hundreds of miles from where the virus was endemic. That was the smoking gun. It was concluded that the virus arrived there not by bat migration, but was carried there in infected animals by traders who sold the animals in the market. Wildlife animal traders were responsible for the fast appearance of the CoV-1 virus so far away.

The Recent Study. Seventeen years after the first SARS pandemic began in 2002, another coronavirus, CoV-2, suddenly appeared and infected people in Wuhan, China launching the COVID pandemic that ravaged the world and is still with us. Like CoV-1, CoV-2, also first appeared several hundred miles from where coronavirus-infected bats are found. How did the virus get to Wuhan? Was it carried by bats whose average home range is about ½ mile and are not migratory (unlikely)? Was it created and released from the lab in Wuhan that did research on coronaviruses, or, like CoV-1, did it arrive with animals brought to the city by animal traders? New research published in the May 2025 edition of the journal Cell indicate that animal traders brought the CoV-2 virus with them along with the animals they sold in the live market.

In the study, an international team of researchers mapped the evolutionary and geographic history of coronaviruses by first sequencing the genomes of 248 coronaviruses from bats. They then compared the genetic similarities and difference between all the different viral genomes to the known genome sequences of CoV-1 and CoV-2. From these data, they were able to use evolutionary modeling techniques to reconstruct relationship trees and dissect the evolutionary history of the coronaviruses that cause both SARS and COVID. The researchers then showed that the spread of the CoV-2 virus doesn’t support natural dispersal by the native horseshoe bat host, or its creation in a lab. They instead found that CoV-2 dispersion mimicked that taken by CoV-1.

As coronaviruses infect animals, different types of the virus sometimes ended up inside the same cell. When the cell makes new viruses, it can accidentally create viral hybrids that carry genetic material from both of the different coronaviruses. This mixing of the genetic information is called recombination. Flu and other viruses are very capable at recombining and forming novel mosaic viruses. It turns out, coronaviruses are pretty adept at recombination too and they use the same genetic regions to repeatedly recombine over eons of time. Therefore, in order to examine the relatedness of the different bat coronaviruses, the researchers focused on regions of the genome that were not involved in such recombination in order to more closely follow the same evolutionary history of each genome and compare that to the non-recombinant regions (NRR) of CoV-1 and CoV-2. The sequences of all so-called “non-recombinant regions” or NRRs were compared and from the mutations identified in each region, a “molecular clock” was determined in order to date the emergence of each viral variant.

The data showed that ancestors of both human coronaviruses circulated in bats across much of Southeast Asia for thousands of years. The horseshoe bat species that hosts the coronaviruses has been around for over 13 million years. So the virus had a constant host in which to mix and mutate.

In 2001, just a year before the SARS pandemic started in Guangdong, the Cell paper reports that CoV-1 underwent its last genetic mixing in bats. And since Guangdong is several hundred miles from the ancestral region of CoV-1, infected bats would not have been able to bring the virus to the region in just a year. Instead, researchers generally agree that this CoV-1-similar virus from bats infected wild mammals that were later transported to Guangdong for sale in the city’s live animal markets. A few months after the start of the SARS pandemic, researchers discovered CoV-1 in palm civets and other wild mammals for sale in those markets.

The researchers also found a similar evolutionary and dispersal pattern when they examined CoV-2 and its related coronavirus sequences. The last recombination in bats took place between 2012 and 2014, just five to seven years before the COVID pandemic began in Wuhan several hundred miles to the Northeast. Researchers believe that, as with CoV-1, a predecessor to the CoV-2 virus entered and circulated in wildlife, which were then transported by traders to Wuhan for sale in its live markets. This explains how the virus could travel such long distances in a short time. This evolutionary pathway is wholly inconsistent with a lab origin for the CoV-2 virus.

The researchers argue that these new research findings agree with earlier studies that they published in 2022 and which were described in these pages. Those studies provided evidence that the Huanan Seafood Market, one of four live markets in Wuhan, was where the COVID pandemic began. Wild mammals were sold there and all the earliest cases of COVID were centered around that market and not around the other markets or around the lab, which is seven miles away from the market. Chinese researchers also collected related strains of CoV-2 carrying a few distinct mutations from the market stalls and wastewater. In fact, the researchers concluded that the pattern of these mutations showed that the virus had twice spilled over to humans from wild mammals at the market.

However, at the end of 2019 when it was first suspected that the market might be the source of a novel pneumonia, wildlife vendors at the Huanan market quickly removed their animals from the stalls before scientists could study them. And once China put a stop to wildlife sales, traders and farmers culled their animals so they could not be tested for the virus. That is part of the reason why the CoV-2 smoking gun (i.e., an animal infected with CoV-2) has been so hard to find.

Bottom line. While this recent evidence is consistent with an animal origin of the CoV-2 virus, it still is not definitive proof. But, this research adds to the growing circumstantial argument that the virus migrated from a bat into wildlife that was sold at the Wuhan market. A “smoking gun” remains to be found to prove with certainty an animal vs lab origin for the virus. Note that it took 30-some years to find the source of the HIV virus, and we still do not know where the Ebola virus came from. So, we keep looking for unequivocal evidence to prove the origin of CoV-2 while realizing we might never find a smoking gun and will have to rely on the preponderance of evidence, which so far favors the animal origin of CoV-2.

COVID: Don’t Touch My Junk

"It's not hard, (it's not hard)"

–from the song, Piano, by Ariana Grande

 

COVID is very strange. Earlier I reported that the SARS-CoV-2 virus, which causes COVID-19, a mostly respiratory disease, also messes with one’s gut health. Elsewhere in these pages, I have also discussed the relationship between COVID and new-onset diabetes type 1, Parkinson’s disease, cancer, dementia, and cardiovascular problems. That is quite a panoply of symptoms unrelated to respiratory disease. We now can also add to that complex array of health problems caused by a respiratory virus, broad effects on the male reproductive system. Ouch!!

Several reports (here, here and here) together report that COVID-infected men often complain of the following several symptoms related to male genitalia:

• Testicular pain
• Erectile dysfunction (ED)
• Reduced sperm count
• Decreased fertility
• Smaller penis size
• Decreased sexual drive
• Swelling
• Prolonged erection

How in the world does a respiratory virus affect all this in the male reproductive system to cause what is sometimes referred to as “COVID penis?” 

Well, we now know that the organs of the male reproductive system, including the prostate, testicles, and penis actually can be infected by the COVID virus and, thus, have their functions compromised. This can lead to erectile dysfunction, decreased testosterone, and reduced sperm levels in 60-75% of infected patients (see here, here)

The fact that a respiratory virus can widely infect men’s junk recently was shown by research from Northwestern University. The study used body scanning technology to surprisingly show that the CoV-2 virus had infiltrated the entire male genital tract of infected monkeys (including the prostate, persimmons, and tallywhacker). From these results, the investigators concluded that the manifold reproductive problems linked to COVID-19 are not secondary effects of fever or inflammation but rather a direct result of the virus infecting cells throughout the male reproductive system. It is believed that CoV-2 infection of reproductive tissues can make the organ’s small blood vessel linings not function properly, which then causes reduced blood supply leading to ED, maybe shrinkage, and the other consequences.

Medical researchers at the University of Florida Health found that men with COVID-19 were more than three times more likely to be diagnosed with erectile dysfunction than those who didn’t have COVID.

A July 2024 review of 16 articles involving 1250 men with active or recent COVID infection  and 1232 healthy controls confirmed that sperm count and motility are significantly reduced in infected men. The results also showed reduced testosterone levels and abnormalities in other hormones affecting sexual function. The fact that COVID has such broad effects on the male reproductive system raises a concern that the disease could be sexually transmitted. Fortunately, no COVID mRNA was found in the semen of any of the infected men, which suggests a low possibility of sexual transmission of the virus.

Another question all of this raises is how long do these effects on men’s reproductive health last. The good news is that two studies published in 2023 and 2024 showed that the reduction in sperm count caused by COVID was transient. Sperm returned to normal levels and motility 3-6 months after infection. How long other problems persist is less  at this time.

All of this information provides yet another good reason to make every effort to stay current with the COVID vaccinations.

It is not hard.

This Post Is For The Anti-Vaxers...

If you think vaccines are more dangerous than the illness the viruses cause, then feel free to avoid them. But read this testimony from Judith Pantages first....

When I was a respiratory-therapy student, we had an iron lung in our lab as a vestige of our field’s history. I thought at the time: I have to get into it to feel what it was like. So I did. It was the scariest moment of my life. I couldn’t ask for help as the mighty negative pressure overtook my feeble effort to breathe. Then there was the claustrophobic effect of being enclosed up to my neck in a steel tube. It probably wasn’t the smartest thing for a student to do, but it gave me deep appreciation for my patients who were polio survivors.

Today negative pressure ventilators have given way to positive pressure ventilators and other noninvasive methods. Still, being on such a thing is no picnic. I wish all those skeptical of vaccines would spend a few moments in an iron lung. Perhaps that would be enough to give them pause.

In other words, get your shot....

 

ALERT!

Hi folks,

Thanks very much for following this blog on the COVID pandemic. I have a couple of topics in production that will soon be posted. I also have been distracted by writing two books, one of which should come out in a few weeks, and the second one based on this blog.

Also, for those of you who follow me on Facebook, know that I have had problems with that account and had to set up a new one. I am trying to regain all my former friends. So, if you were a Facebook friend, or want to be, please send me a request to:

https://www.facebook.com/profile.php?id=61573910458533

SARS-CoV-2, A Respiratory Virus That Messes With Your Gut

The CoV-2 virus that causes COVID is a respiratory bug, right? They say we catch it, not from surfaces or food, like we do norovirus, but from airborne exposure—we breathe it in. That of course, means that it causes respiratory problems. Makes sense, right? Well, Sarah Carter, 36, from San Mateo, CA, caught the virus in late 2023. Her main symptom was not respiratory but relentless diarrhea that became so sever she had to take an ambulance to the ER. The runs caused her to become dehydrated, which in turn caused a spike in her blood pressure and heart rate. She urgently needed IV fluids to treat it all. After three more days of diarrhea she finally felt better. But, six months later the GI symptoms reappeared overnight without her being infected again. Nearly everything she ate set off diarrhea. She also had bloating and pain so severe that she said it felt like acid was running through her intestines. A gastroenterologist eventually diagnosed her with post-infectious irritable bowel syndrome (IBS).

What in the world is a respiratory virus doing messing with her entrails, especially months after being infected? Did it make a wrong turn somewhere?

We have gotten accustomed to testing for COVID when we feel crummy and run a temperature, have a sore throat, runny nose, loss of smell, cough, etc.—all symptoms of respiratory infection. But Dr Rohit Jain, an internal medicine doc at PennState Health told Time that when someone complains of problems affecting the exit at the other exit of the body: i.e., nausea, diarrhea, vomiting, etc., he always tests for COVID. Another doctor, Mark Rudd, chief of infectious diseases at the U of Nebraska Medical Center also weighed in saying that, “COVID-19 is really a GI-tract disease.”

What??

If it “really is a GI disease” why are we wearing masks, distancing, and worried about respiratory infection rather than hand washing and sanitizers??

The SARS-CoV-2 virus and its disease, COVID, are very strange and threw the medical establishment for a loop after they first appeared on the scene at the end of 2019, and after COVID became a world-wide pandemic in early 2020. Docs dealt with myriad, seemingly unrelated symptoms in different patients; symptoms such as brain fog, loss of smell, severe pneumonia, hemorrhage issues that led to black toes and lungs that looked like they had filled with chocolate pudding, among many others; all from the same virus. Now add to that befuddling mix, GI problems to what was believed a respiratory virus,and COVID presents a conundrum. Docs have to now factor in the fact that many people experience no, or only mild gastrointestinal symptoms, while other patients experience significant digestive problems that can distract from the pulmonary problems which complicate diagnoses.

As we have learned more about COVID over the last few years, it has become clear that infection symptoms can also include loss of appetite, nausea, vomiting, diarrhea, and stomach pain, according to Jain’s research. A 2023 study published in Nature Communications reported that 36% of COVID patients are likely to develop GI disorders such as ulcers, pancreatitis, IBS, and acid reflux. Another recent study in Clinical Gastroenterology and Hepatology found that 40% of adults hospitalized with COVID, had at least one GI relapse a year or more later. While both of these were small studies, they are in close agreement regarding the incidence of COVID GI problems. And like other symptoms of long COVID, the GI problems can last many weeks. That is quite concerning. Weeks of diarrhea, for example, is much more than an immense inconvenience and major mess, it is a serious medical issue. But not all patients experience these symptoms, just like not all patients lose their sense of smell, had black toes, or developed long COVID. Try to diagnose and understand COVID with this range of variable symptoms! How confusing.

How can the same virus cause runs from both ends of the body; the nose and the other end?  Among the things we have learned over the last few years is that the CoV-2 virus infects cells that express the ACE-2 protein. While ACE-2 normally is important for certain cell functions, the virus decided to use it as a receptor on which to grab onto and then enter cells. The protein is found on many different types of cells throughout the body, but it is expressed in especially high levels in the lungs, which helps explain COVID’s respiratory symptoms. It turns out that ACE-2 is also highly expressed in cells of the GI tract. That explains the intestinal complications. Also, because it is found in the GI tract that could possibly make feces from infected animals, like bats, a great way to widely spread the virus to other animals, just like migrating birds spread the avian flu virus to poultry flocks and dairy herds. In fact, in 2012, six Chinese mine workers removing guano in a bat-filled cave where flying flittermice were found with COVID, developed severe respiratory symptoms. Three of them died. COVID infection from contaminated bat guano is suspected because the Wuhan lab eventually found evidence of an unknown coronavirus in the patient samples. But, this was years before the CoV-2 virus had been discovered, so the CoV-2 link to their disease comes with some uncertainty. Maybe the virus in ca-ca could be a way to spread it between people too, like norovirus is spread. To my knowledge, human-to-human spread this way has not been shown, but it makes sense to this scientist that it could. After all, since the virus is found in feces, wastewater surveillance has proven to a useful tool for tracking CoV-2 spread among human populations. It is routinely found in poop, and there is a good possibility that the Chinese workers caught it from the bat scat they were shoveling. Together, that makes it very likely that humans can spread it to other people via unsanitary practices. But, at this time, that is just the opinion of your sometimes humble correspondent. We will see.

We also now know that the virus can hide in the nooks and crannies of the  bowel for months, or even years, according to Ziyad Al-Aly, MD, an epidemiologist at the Washington University School of Medicine in St. Louis, who co-authored the Nature Communications study on chronic post-COVID GI symptoms that was cited above. This might explain why gut-related symptoms can long outlast the initial acute infection. But other possibilities to explain long-COVID GI problems continue to be investigated. This is another “we shall see” issue.

We also know that the virus can cause widespread and sometimes long-lasting inflammation, potentially affecting various organs throughout the body including the gut. GI inflammation can affect the gut microbiome, which is the collection of microbes that normally live in the GI tract and that are good for us. We have long known that changes in the gut microbiome can have manifold health effects affecting GI health, and even the well-being of the heart, kidneys and brain, including Alzheimer’s disease, which is a possible complication of COVID. Disruption of the GI microbiome also is related to obesity and diabetes and it is notable that COVID disease also is associated with new-onset diabetes. Inflammation in the gut can also damage the lining of the intestines, making them “leaky” so that nutritional goodies from foods you normally would absorb across your gut into the blood stream, instead escape into the abdomen, causing immune cells to mount an allergy-like response to foods. COVID-induced inflammation can also chew away at the nerves that control normal gut contractions (peristalsis) that move food along, and interfere with neurological signals in the gut causing pain. Not fun, ask Sarah Carter!

Since the start of the pandemic in early 2020, GI docs have noticed an uptick in IBS in COVID patients. Medical scientists have long known that other gastrointestinal infections, like those from norovirus, giardia (a parasite), or salmonella (bacteria), can lead to IBS as well as functional dyspepsia, a type of chronic indigestion that causes frequent feelings of fullness and stomach pain or burning, like acid running through your innards. Does that sound familiar? Now we can add the respiratory virus, CoV-2, to the list of infectious agents that can cause IBS and other digestive problems.

Bottom line: So, gut problems are added to the manifold issues associated with COVID disease. CoV-2 is a nasty bug that you don’t want to catch. Get vaccinated and spare yourself all these problems!

Over 400 Studies Show Face Masks Protect Against Respiratory Infection

“Sometimes we need education in the obvious more than investigation of the obscure.”

–Oliver Wendell Holmes

In my meanderings across the blogosphere, opinion pages, talk radio, Facebook, and even chatting with friends and acquaintances, I continually encounter folks who assert that masking is ineffective for protection against respiratory infections. Of course they never provide evidence to support their claim beyond their confidence that they are correct. I often reply that they should invite their next surgeon to remove his mask during the operation. I have published in these pages a few articles showing how controlled trials and real-life empirical data show this to be wrong (see here, here and here).

Now a new meta-analysis by University of Oxford researchers, or an analysis of some 400 published studies on facemasks, further confirms that if they are correctly and consistently worn masks effectively protect against respiratory infections, including COVID. The study also concludes that mask mandates are effective in reducing community transmission of respiratory pathogens. Note that health mandates have long passed Constitutional muster as I reported earlier. This new analysis was triggered by the controversial 2023 Cochrane review of non-pharmaceutical interventions for COVID, which several publications reported showed that masks were ineffective. However, Cochrane’s editor-in-chief later stated publicly that the review did not support such a conclusion and issued an apology for the confusion and a clarification. Several scholars also questioned the review’s methods and found flaws in its meta-analysis and criticized it for omitting a vast body of non-trial evidence. Hence the Oxford study was undertaken to learn the truth about the efficacy of face masks.

Face masks, along with other non-pharmaceutical measures, such as social isolation, have long been used during infectious epidemics, especially when vaccines and antibiotics were not available. This goes back to the European bubonic plague in 1619, the Great Manchurian plague (1910), the 1918 Spanish flu, etc. When there is no vaccine or therapeutic intervention to treat an infectious disease, physical isolation measures, such as social distancing, quarantine, and masks are critical.

The Oxford study. The study examined the relevant literature in a wide range of disciplines (public health, epidemiology, infectious diseases, biosecurity, fluid dynamics, materials science, modeling, data science, clinical trials, sociology, anthropology, psychology, and occupational hygiene). This included numerous randomly controlled trials as well as observational, or “real-world,” evidence. The results convincingly showed that cloth face coverings and disposable medical masks that are handed out at your doctor’s office can reduce infection risk, but the N95 respirators are much better.

In the early COVID-19 pandemic, when randomly controlled trials of masks had not yet been done, the study’s authors found a systematic review and meta-analysis of observational studies reporting that respirators and masks decreased infection risk up to 85%. Further, in a school-based cohort study, the risk of COVID among the family members of students was reduced by 30% to 40% when teachers used masks.

Other case-control and cohort studies in healthcare workers provided additional evidence of substantial reductions in COVID-19 risk associated with use of respirators. In 2020, one study found over 400-times lower odds of occupational acquisition of COVID among hospital staff using N95 respirators in respiratory, intensive care, and infectious diseases departments compared to those from other departments without continuous masking.

While cloth face masks were proven to protect against airborne infection, N95 or FFP2 face-fitting respirators were most effective. The latter fit more closely to the face minimizing ambient air from leaking through the edges. They also work differently from cloth masks, which use multiple layers as a barrier to block pathogens. In contrast, respirators pass air through a specially designed filter that uses electrostatic charges to trap airborne particles, whether dust or bugs.

The pore size in typical surgical masks and respirators is larger than many viruses, like Cov-2, but, viruses do not float around the air on their own. They are carried as passengers via respiratory aerosols, which are blocked by masks. Note that the International Standards Organization (ISO) provides standards for optimum filtration for respirators. This includes lab testing for filtration efficiency. This also includes personal testing while exercising in the face of a challenge contaminant. A respirator is considered to meet requirements when it achieves a 100-fold reduction in the challenge contaminate penetrating the barrier. Respirators outperform surgical masks by 8-12-fold. These results were further confirmed with animal Cov-2 infection experiments. Infected hamsters were separated from uninfected ones by a partition make of surgical mask material, which reduced Cov-2 transmission by 75%.

Besides lab studies and randomly controlled trials of face mask use, the authors also conducted a systematic review of 44 observational studies involving SARS-1, MERS, and SARS-Cov-2. They concluded that masks and respirators reduced the risk of infection by 85%. Overall, respirators were 96% effective while surgical masks were 67% effective. This protection was “dose dependent,” meaning that protection increased with the frequency of use of masks. Masks were not only found to protect the wearer, but also were effective and preventing infection of non-mask wearers surrounding the masked person. But, the greatest protection was when both parties were masked.

In addition, the study examined the effects of mask mandates in several different settings. The first such analysis found a progressive decline in epidemic growth rates after mandates were enacted when compared to time frames immediately before the mandates. Also, masking was an effective predictor of lower infection rates in the US. An analysis of masking in Boston schools, found a surge in CoV-2 infections after February 2022, when mandates were lifted. Similar evidence demonstrating the efficacy of mask mandates was reported in many other studies. Importantly, the meta-analysis did not find any evidence for significant harm to the health of mask wearers even during strenuous exercise. Specifically, they do not increase the carbon dioxide content of inhaled air. The biggest impediment to using them was discomfort and communication difficulty for deaf people who are unable to read the lips of a mask wearer.

Study conclusions. The claim that masks do not reduce transmission of airborne pathogens is incorrect. They work. Furthermore, the level of protection increases as adherence to masking increases. Masks are a critical part of infection control during a respiratory infection epidemic.

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Infections Can Cause Brain Atrophy And Dementia

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“We could certainly slow the aging process down if it had to work its way through Congress.”
 -Will Rogers

Two provocative areas of research have led to the notion that infection could be a risk factor for dementia. On one hand, some studies have directly suggested that there is a possible link between some infections and an increased risk for Alzheimer’s disease (AD). Then, other studies found that two vaccines, the flu shot and the shingles vaccine, reduced the risk of dementia. Together, all this led to the hypothesis that infection might play a role in neurodegenerative diseases. This is now bolstered by a new study published last August in Nature Aging that identifies possible post-infection immunological/inflammation drivers that lead to brain atrophy and subsequent cognitive decline.

Brain atrophy! It can easily be detected via modern imaging technology, and it is not good.

We have abundant evidence that even minor infections can change the way we think and behave. More-severe infections that result in delirium have long been associated with long-term cognitive problems. Even shingles, which is a very painful relapse of chicken pox (you never clear the virus, which resides in your nerves) also is associated with dementia. There is a very effective vaccine that stops shingles in its tracks and it has been shown to reduce the risk for dementia later in life by up to 50%. The more severe an acute infection or its relapse, the greater the inflammation caused by the immune response, and the greater the risk of Alzheimer’s and other types of dementia. Therefore, it makes abundant sense that vaccines, which greatly reduce the severity of infectious disease, would also lessen the risk for dementia as well as for other long term post-infection health problems such as diabetes, Parkinson’s diesease, and maybe cancer that I have mentioned in these pages.

The link between infection and cognitive problems seems to hold with different types of infections, whether they are bacterial or viral. Of the 15 types of infections studied, six—flu, herpes (which includes small pox, chicken pox, shingles, etc.), respiratory tract infections, and skin infections—were associated with increased risk of atrophy in the brain’s temporal lobe. This region includes the inner folds of the temporal lobe where a rather small organ called the hippocampus sits on each side of the brain. This is part of what is called the limbic system, which manages the functions of feeling and reacting, and helps us process and retrieve two types of memory, declarative memories and spatial relationships.

Declarative memories are those related to facts and events such as learning how to memorize speeches or lines in a play. Spatial relationship memories involve pathways or routes. For example, when a cab driver learns a route through a city, they use spatial memory and that learning can actually increase the size of the hippocampus. Spatial relationship memories appear to be stored in the right hippocampus. In addition, short-term memories are converted into long-term memories in the hippocampus, but are then filed away long-term elsewhere in the brain. So, with a malfunctioning hippocampus, these short term memories do not get stored. And we forget things.

We have known about the hippocampus (or hippocampi, since we have two of them) for more than four centuries. The surgeon, Julius Caesar Arantius, first discovered the hippocampus in 1587, coining the term from the Greek word for seahorse (hippokampos) based on its shape. It does resemble a seahorse. This region, critical for memory and learning, is strongly affected in AD where the shrinking size of the hippocampus can be used to monitor the progress of the disease.

The latest study relating infection to dementia was based on data from the Baltimore Longitudinal Study of Aging, one of the longest-running studies of human aging in the United States. They also used neuroimaging to track how brain volume changed in 982 adults, with or without a history of infection. This began in 2009 and its data confirmed findings from analyses of UK Biobank data of almost 500,000 people, and a Finnish dataset of almost 300,000 subjects, both of which identified these infections as risk factors for dementia.

Of course, most of these studies were done before COVID. COVID has not been around long enough to definitely tell us whether the disease is also linked with increased risk of dementia, but as a respiratory infection accompanied by severe systemic inflammation, we can expect it to be.

Bottom line: Vaccines not only protect against the acute infection they were made for, but they also protect against serious post-infection complications such as new onset diabetes, Parkinson’s disease, perhaps cancer, and other long term complications of infectious disease, which now also includes dementia.

Get vaccinated!

COVID On The Heart

“We will see….”

I often end these blog posts that describe the confounding nature of this brand new SARS-CoV-2 virus and its novel disease, COVID, saying, “We will see.” The virus and its disease, both, have been very unusual and medical science has been continually trying to catch up with it and understand new issues they present. Hence, novel information we have been gathering takes a while to understand, so "We will see" is an appropriated disclaimer.

After four years dealing with all this, our vision is gradually improving. For instance, we are getting a better handle on how infection with the virus affects the heart.

Sadly, too many armchair medical conspiracists still frequently sound off that mRNA vaccines are causing thousands of deaths due to cardiovascular problems they cause. They do so without ever proffering credible evidence to support their notion--they simply claim that it is self evident. The truth is that the vaccines are not doing that in any significant number as I previously debunked here, here, here and especially here. Several clinical trials done before the vaccines were released demonstrated that cardio risk from the shot is negligible, and when it occurs it is inconsequential and usually accompanied by no symptoms. It is just detected via blood test. This has since been confirmed in a billion people around the world who have gotten several billion shots as investigators continue to follow the outcomes of vaccinated people in what are called, “post-market studies” or "phase 4 trials." Rather, it is the virus that is causing almost all the cardiovascular problems and this is well established by the research.

We do know that between March 2020 and March 2022, there were ~90,000 more cardio deaths in the US than expected. Most of these were in people 65 and older who have the highest risk for such problems, but heart-related deaths also jumped dramatically for healthy 25-44 year old COVID patients. How does the virus do this?

It is understood that CoV-2 infection and COVID disease cause widespread inflammation in the body, the vaccines, not so much in most recipients. General inflammation caused by viral infection is what increases cardio risk. The virus and disease stick around a while and so does the inflammation; the vaccine and its side effects do not. The immune system responds to this lasting infection, in part, by releasing hormone-like proteins that cause inflammation and blood clotting. Clotting and plaque accumulation in arteries lead to heart attacks or strokes. Smokers and those with high blood pressure often already have plaque in their arteries, so it is no surprise that these folks are at the highest risk for COVID-caused cardiovascular problems.

Even without pre-existing plaque, virus-induced inflammation in blood vessels alone can lead to clot formation, even in the absence of other high risk factors. That helps explain how younger, healthier people also show increased risk for cardio problems after infection with the virus.

We have also learned that even if you had COVID a year ago and cleared it, you remain at long-term risk for all cardiovascular problems according to a large study that analyzed medical records of almost 700,000 patients. The stroke risk is 1.5 times elevated; risk of heart attack is doubled; and the risk for different types of arrhythmias increases 1.6-2.4 times. Some of this elevated risk comes from the ability of COVID disease to induce new-onset high blood pressure in some people. Why this particular consequence to infection happens is another “we will see” question.

The good news is that vaccines reduce all this risk. Other studies showed that people who are vaccinated are roughly 40 to 60 percent less likely to have a heart attack or stroke following a COVID infection than those who are unvaccinated. This may be because vaccinated people are less likely to develop severe COVID. The greater the severity of disease means that the patient experiences much more inflammation which in turn leads to greater risk of cardio problems.

Again, the risk of the vaccine causing myocarditis is way overblown and those who continue to harp on this are spreading disinformation. The risk of myocarditis following infection is 4-8 times greater than following the vax, not the other way around. Don’t believe these lies, which cannot be supported by medical science, only by salacious rumor.

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