I normally drink 100-150mg/day, but I had to cut that back to 50-60mg and only in the morning. It seems to have passed, so I'm back on my drip.
You can also find some good decaf black tea. Jones Coffee Roasters in Pasadena stocks some, and I'll see it online occasionally.
This doesn't mean that AMPA receptors are the root cause of post-COVD brain fog, nor does it necessarily mean that drugs modulating AMPA receptors could reverse it. It only shows that this is one of the changes observed in patients reporting post-COVID brain fog. It could be a side effect of some other change or it could be part of a long cascade of changes.
It also needs to be replicated further. I've read at least at dozen headlines claiming to have found the underlying cause of COVID brain fog in the past year and all of them pointed to different biomarkers.
Consider this another piece of the puzzle, not a discovery of the underlying mechanism.
It doesn’t say root cause, or drug target. It doesn’t say reverse or cure. It quite specifically doesn’t say “the basis”. The word basis doesn’t have to refer to one root cause. It could be something foundational, but there can be many elements of a foundation. It certainly isn’t the entire structure.
I’d argue it’s quite tame as academic press releases go.
The headline quite specifically does say: "Uncovering the Molecular Basis of Long COVID Brain Fog"
The article also implies that AMPA drugs could address COVID brain fog:
> For example, drugs that suppress AMPAR activity could be a viable approach to mitigate brain fog.
This was one of the points I was trying to counter.
It also claims to have "resolved key uncertainties":
> In summary, the team’s findings resolve key uncertainties about the biological basis of Long COVID brain fog
Which is obviously not true. This is only one biomarker, not the resolution to a key uncertainty.
I disagree that I'm reading too much into it. These are direct quotes from the article I was responding to.
You are welcome to your opinion about what is key, but reading comprehension does not seem to be your strong suit.
> "the [...] Basis"
The adjective molecular doesn't narrow "the basis" down much, for a condition which could safely be assumed to be molecular.
Which can still be extremely useful, for targeting further investigation.
It's the university PR team that exaggerated, as usual.
On a long covid news article? What are the chances!
I'd also remark that their methodology has issues; we do not have a clear etiology or diagnostic criteria for "long covid" and its presentation. Participants had previously been infected (this is essentially everyone) and reported subjective "brain fog" type symptoms which is a terrible way to attempt to isolate anything about this "long covid". It's possible this is just a generalized syndrome that results from behavioral or lifestyle factors. I.e. we have no way to know what is "long covid" versus other things, no way to reliably trust patient history, and no way to know we are seeing that particular type of "brain fog".
It does not necessarily.
For example, if the increased AMPA density is a counter-regulatory response to reduced baseline AMPA activation, further antagonizing the receptor system would worsen rather than improve the situation.
As for tolerance, I haven't noticed the brain fog come back since I started, and I've been on this for 6 or 8 months so far.
I've never smoked cigarettes, but decided to try Nicorette gum as an alternative to a second cup of coffee (if I drink after 12:00, I wont go to sleep on time).
I've been using it for 8+ years now and have found a sustainable dosage that doesn't give me withdrawal/depenency. I've never had an issue with tolerance.
I buy a big box of 4mg gum and go through around half to one piece a day. I discovered consuming 2+ pieces (+8mg) led to withdrawal symptoms (empathetic lightbulb moment for me for smokers who want to quit!)
Regarding dependency, I don't take any when Im traveling/on vacation, and have never felt the need to use it then.
Any desire comes from wanting to continue the alertness once the caffeine starts to wear off.
> Any desire comes from wanting to continue the alertness once the caffeine starts to wear off.
Anecdotally, this sounds a lot like two of my friends (married couple) who used similar amounts of nicotine gum years ago.
For years they said the same thing: That they didn't go into withdrawals on vacation and that they weren't addicted to the gum, they just wanted to feel awake.
Their experience changed when they decided to quit for a while. As they discovered, actually quitting for an extended period of time was a lot harder than they thought it would be.
They were very much in the "I can quit whenever I want" mindset because they could skip it on vacations, but as they discovered their cravings were intense when they tried to go without the gum during their normal weekly routine.
They finally tapered down with the lower doses and splitting gum over a long period of time.
I vape like a fiend and I'm probably never going to stop
If you like smoked food, you'll love the taste of smoking. Though, I highly recommend limiting it to serious celebrations, for obvious reasons. I generally only have them at weddings.
https://pmc.ncbi.nlm.nih.gov/articles/PMC11336094/
I would be curious if these markers could result from the same problems, or might indicate a complete separate root cause.
marstall•3mo ago
Aurornis•3mo ago
The study only looked at one marker. It doesn't confirm that increased AMPA receptor density is the cause of decreased cognition. It only suggests that decreased cognition is correlated with increased AMPA receptor density.
There are many processes in the body where reduced activation of a receptor system results in an increased number of those receptors. So don't conclude that this is the reason why patients have brain fog. I would guess it's just more of a symptom than a cause until there's more research
lenerdenator•3mo ago
Just a shot in the dark here, I'm just some guy on the internet, not a microbiologist or doctor.
dekhn•3mo ago