A possible treatment for long Covid brain fog 

A small study has identified two drugs, guanfacine and N-acetylcysteine, that may offer help for long Covid’s brain fog. In some cases they decreased it and in others flat-out eliminated it. And because  the drugs have already been approved for other uses (at least in the US, where the study was done; I’m not issuing guarantees about other countries), patients should be able to get them if they can find a doctor willing to prescribe them. 

Please note the if and the should in that sentence. It’s possible but not guaranteed. 

The results were strong enough that one of the researchers, Arman Fesharaki-Zadeh, went from researcher to advocate. 

“There’s a paucity of treatment out there for long Covid brain fog,” he said, “so when I kept seeing the benefits of this treatment in patients, I felt a sense of urgency to disseminate this information. You don’t need to wait to be part of a research trial. You can ask your physician—these drugs are affordable and widely available.” 

To confirm the findings, larger trials will have to be done, with a control group taking a placebo and lots of people in white lab coats looking important, but Fesharaki-Zadeh was convinced enough by the improvements that he’s gone on to use the combination with people whose symptoms are similar but were caused by Lyme disease and MS. He says the results are promising.

Irrelevant photo: Daffodils in February.

Other long Covid news

I’ve seen several articles lately about long Covid’s impact not on individuals but on society as a whole. The U.S. Government Accountability Office estimates that it has affected somewhere between 7.7 million to 23 million Americans. That’s a hell of a range, which probably testifies to how badly defined long Covid still is. 

A different study estimates that 500,000 people in the US aren’t working because of long Covid.

“It’s a pretty conservative estimate,” according to Gaurav Vasisht, a co-author of the second study. “It’s not capturing people who may have gone back to work and didn’t seek medical attention and may still be suffering, so you know, they’re just toughing it out.”

The good news is that the number of long Covid cases as a percentage of workers’ compensations has decreased. That change coincides with vaccines and treatments that can reduce the risk of long Covid becoming available.

What treatments? The article didn’t say, damn it. My best guess is they’re talking about antivirals.


A different study reports that in people whose mild Cofid cases left them with long Covid, the “vast majority” of the symptoms clears up after a year, and that vaccinated patients had a lower risk of breathing problems. 


Ah, but we have to balance out the good news, don’t we? A study that looked at a range of other studies saw that although most long Covid patients with mild cases recover, that’s not true of people with severe cases. 



Yet another study shows a healthy lifestyle coinciding with an almost 50% reduction in the chances of women getting long Covid. That’s not proof that the two are linked, only a bit of statistical flag-waving that says these two things live together, eat supper together, and leave for work together, so we could maybe assume they’re in a relationship, not just roommates. 

The lifestyle (damn, I hate that word) factors they took into account were maintaining a healthy weight, getting enough sleep, not smoking, drinking only moderately, exercising, and eating a good diet. 

Swearing seems to have no impact, one way or another. 

The slightly-more-than-half the group who did get long Covid got milder cases. 

Why did the study focus on women? The article didn’t say, but women are somewhat more susceptible to long Covid. That may or may not explain it. 


Vaccine news

India has become the first country to approve a nasal Covid vaccine. It can be used as both a booster and a primary vaccine. Because the vaccine sets up shop in the nasal cavities, which is where Covid likes to set up its own shop, it could keep Covid from spreading. Could. Potentially.

Watch this space. Watch several other spaces. Watch your nasal cavities. We’ll see what happens.


In China, researchers are at the animal testing stage of what they hope will be a universal Covid vaccine that targets a portion of the virus that has stayed stable across multiple mutations–11,650,487 of them if you’re counting. I’m not. I ran out of fingers somewhere around 12.

It needs more testing before it goes to human trials, but if I understand the article correctly, they’re hoping it will prevent breakthrough infections–the kind that dog people who’ve gotten the current vaccines. In other words, it could actually halt the spread of Covid–which (in spite of the way 90% of the people we all know are acting) ain’t over.


Non-vaccine news

We’ve got two items in this enticing little basket:

Number one is a spray that–if it works, of course–could keep Covid from getting any further than our breathing equipment. A group of engineers created “thin, thread-like strands of molecules called supramolecular filaments.” The idea is that you spray ‘em in your nose (or possibly mouth) and they block any virus from getting into your lungs.

Yes, you can still breathe through them.

The effect may only last an hour or two, but it would allow you to go into your nearest overcrowded venue and forget your worries for a while

How does it do that? Um, well, yeah. What do you say I quote?

“The filaments carry a receptor called angiotensin converting enzyme-2, or ACE2. These receptors are also found in cells in the nasal lining, the lung surface, and small intestine, and have many biological roles, such as regulating blood pressure and inflammation. The novel coronavirus enters our bodies primarily through interactions with this receptor. The virus’s characteristic spike protein clicks into this receptor, much like a key going into a lock, allowing it to enter the cell and replicate. Once the virus is locked into the cell, it prevents the cell from executing its normal functions, leading to and exacerbating infections.

“Researchers have long known that adding extra ACE2 into airways can block virus entry, essentially preventing the virus from binding with ACE2 in the lungs. However, since ACE2 has biological functions, simply delivering more ACE2 to the body may have unforeseeable complications. The research team’s newly engineered filament, called fACE2, serves as a decoy binding site for the virus, with each filament offering several receptors for the COVID-19 spike protein to attach to, and silences ACE2’s biological functions to avoid potential side effects.”

Like so many of the innovations I write about, though, it’s not yet ready for prime time.

Item number two in the basket is–oops, it’s very much the same but it’s coming from a different group. In fact, from more than one different group but still involving ACE2 receptors, decoys, all that stuff. 

Different delivery systems, different colors, slightly different mileage, but once you get past that they’re all related. Something seems to be happening here. Keep your eye on it.



Statistically speaking, what do we know about the pandemic? 

  • That at least 6.8 million people died of Covid and 752 million caught it. 
    • That those numbers massively undercount what happened. Multiply them by 2 or 3 and you’ll get a more realistic number. 
  • That the global GDP dropped by 3.1% in 2020. Compare that to a 1.3% drop during the 2009 crisis. It bounced back by 5.9% worldwide in 2021.
  • That 135 million jobs were lost in 2020. 
  • That in 2022, 56 million more people were out of work than before the pandemic, and 37 million are expected to still be out of work in 2023. How those numbers square with the 5.9% bounceback in GDP is anyone’s guess.
  • That in the US, Covid is the eighth leading cause of death among people between 0 and 19 years old. If we limit that to disease-related deaths, it’s the fifth, and it’s first among infection or respiratory diseases.

Sorry about the wonky spacing of the bullet points. I’m sure there’s a way to even them out but I haven’t found it.


A study of Covid in California prisons–do I need to mention that they’re crowded?–shows that vaccination and boosters reduced the spread of the omicron variant by 11% for each additional dose.

For the mathematically impaired, I’ll point out that 11% is not 100% but it’s also not 0%. That means breakthrough infections–the ones that push their nasty way in among the vaccinated–were common but they were less common than Covid cases would be without vaccinations. And the rate of serious illness was low.  In a bit more than five months, they clocked 22,334 confirmed omicron infections but only 31 hospitalizations and no Covid deaths.

People who’d been vaccinated were a bit less likely to transmit the disease–the number dropped from 36% to 28%–but the longer it had been since a person was vaccinated, the more the chances of transmitting the beast grew–6% every five weeks. People are at their least infections within two months of being vaccinated or getting a booster.

Having said all that, Covid was spreading widely in the prison population and Sophia Tan, the study’s first author, was calling for “new ideas. . . since the risk of infection in this vulnerable population remains so great.”