Hello Long Hauler fam,

☀️ Here are 3 research findings, 1 thought, and 1 question to consider this week - plus a doggy pic 🐶

3 IDEAS FROM RESEARCH

I. Good review of low-dose naltrexone - but still waiting for a proper trial

On 16 July, BMJ Open pooled every published Long Covid study of low-dose naltrexone: four studies, 155 people.

LDN is well known anecdotally to long haulers – a reasonable chunk of people report benefits (although not everyone, and some find they have to start at ultra low doses).

The numbers look encouraging. Moderate improvement in fatigue (Hedges’ g −0.74), brain fog (−0.53) and sleep (−0.60), with pain and daily functioning moving further at −0.93 each.

BUT note that none of the four studies was randomised or placebo controlled. All were before-and-after: measure people, give them LDN, measure again. The authors say that design “precludes causal inference”, and that the improvements “could reflect the natural history of the illness, regression to the mean or placebo effects”. They rate the evidence low certainty.

Still - something happens when people take LDN, consistently across four separate groups.

Good news - a proper trial is coming - RECOVER-TLC’s Brave-LC.

Remember, whether to try LDN is a conversation for you and a doctor who knows your history - check out the online forums for peoples’ experiences and advice.

Sources: BMJ Open meta-analysis · RECOVER-TLC trials, FNIH

II. A German team is going after B cells

The ME/CFS Research Foundation announced seven new projects worth €2.4 million!

One trial, TAME, gives tafasitamab - an antibody that clears out CD19-positive B cells and plasmablasts(!) - to 38 people. I’ve gotta say, loving some of these funky names!

The idea is that in a subgroup of us, B cells produce autoantibodies that keep the illness running.

It’s also open-label, so everyone knows they’re getting the drug and there’s no placebo group. Just like the LDN-reviewed studies, that makes any improvement hard to read.

Source: ME/CFS Research Foundation

III. A properly blinded Long Covid drug trial should be reporting soon

ADDRESS-LC is testing bezisterim (NE3107), a pill that crosses into the brain and quietens inflammatory signalling.

And delight of delights - this study can give us strong evidence: randomised, placebo controlled, triple-blind, eleven US sites, around 200 people with both fatigue and brain fog, twelve weeks of treatment. The main measure is a computerised cognition test.

Admittedly, the trial is run by BioVie, who make the drug (the $13 million funding it came from a peer-reviewed US Department of Defense grant).

Even so, a blinded placebo-controlled trial that has finished enrolling is a different order of evidence from what we usually get. They’re supposed to be writing up the results soon.

Source: BMJ Open protocol

1 THOUGHT

Have a friend who says ‘maybe your muscles are just deconditioned’?

A Nature Communications paper on 28 July put this one to bed (excuse the pun).

It compared people with Long Covid and ME/CFS against healthy controls who’d spent 60 days in strict bed rest (I was curious where these healthy folks came from/why they participated, but couldn’t find out).

Bed rest in healthy people caused muscle shrinkage.

Long haulers’ muscles showed something different: more glycolytic (fast twitch) fibres in both illnesses, and in ME/CFS, selective wasting of the type I fibres - the slow, endurance ones.

The authors’ conclusion: lack of exercise does not explain our reduced exercise capacity in these illnesses (although, of course, we may also be a bit deconditioned).

Next time it comes up over a cup of tea, you have a solid study to point at.

Source: Nature Communications

1 QUESTION FOR YOU

I can feel Spring poking its head around the corner in New Zealand… flowers opening and birds on the wing… And I breathe a sigh of relief to leave Winter behind.

What season do you find easiest for your symptoms?

pooch p.s.

📷 Whisky admires the fresh morning

Alt text: Whisky, the cream coloured toy poodle stares out appreciatively at a frosty glowing river, sun peeking through the branches.

Wishing you a peaceful week,

Tom and Whisky ☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

☀️ Here are 2 research findings, 1 thought, and 1 question to consider this week (plus 🐶 pic)

2 IDEAS FROM RESEARCH

I.

An old drug seems to help some of us.

Rapamycin is an old, well-mapped medicine - normally used after transplants - and it’s been tested in ME/CFS in low doses.

The study found it helped some people by calming inflammation in the brain’s immune cells, and helping the mitochondria work better.

(they took microglia -brain immune cells- grown in a dish, bathed them in patients' blood plasma, and watched what the plasma did. Delightful!)

Of 65 who finished, 26 were classed as responders, 31 as partial responders, and 5 as non-responders.

Interestingly, it was over 2x as likely to help people whose illness began after an infection (including COVID) - a hint that who responds might be predictable.

Big catch though - Everyone knew they were taking the drug, with no placebo group alongside- hope alone can nudge fatigue scores. This needs a proper blinded trial, which the research team is keen to do.

There was a previous (Phase 1) trial of the drug that caused a lot of side effects (many people dropped out)- this time around they seem to have fixed a lot of these issues with a better specific formulation.

For the nerds: the proposed mechanism is chronic mTOR activation, which has been described in a subset of ME/CFS patients

Source: Journal of Translational Medicine (Gile et al) - https://link.springer.com/article/10.1186/s12967-026-08575-3

II.

Brain fog as rinse cycle

A team at Griffith University in Australia scanned the brain’s overnight rinse cycle - the system that clears out waste while we sleep. In ME/CFS, it looked sluggish. And the more sluggish it was, the worse people’s sleep and focus.

For a symptom waved away for decades as “in your head”, seeing it on a scan is satisfying. This is apparently the first study to demonstrate impaired glymphatic function in ME/CFS using MRI.

Caveat: it was a small study, and the gap between patients and healthy volunteers was modest - not everyone’s convinced it’s meaningful yet. Definitely needs a bigger group to confirm.

Still, if it holds, it puts sleep and the brain’s clean-up on the list of things worth measuring, and treating.

Source: Griffith News, published in Frontiers in Neuroscience - https://news.griffith.edu.au/2026/07/03/brains-waste-clearing-ability-impaired-in-me-cfs-patients/

1 THOUGHT

Like many of us I often try different things and have to try and stay quite tuned into my body. Something I’ve been thinking about:

Avoiding getting too cold seems to really help me. It’s currently winter in New Zealand and this year I’ve made an extra effort to stock up. My new favourite is a nice neck warmer that can easily be pulled up to cover my mouth. I know many people who are long haulers suffer from persistent coughs. For me this is made much worse by cold and I’ve found covering my mouth seems to help a lot (means you breathe in warmer air. Bonus when it’s a cute fluffy merino wool fabric!

Of course, getting too hot is also a big problem! It’s a balance….

1 QUESTION FOR YOU

Is body temperature regulation something that you struggle with? Any favourite ways of managing it?

puppy p.s. Important gardening work

[alt text: Whisky the cream coloured poodle and Monty the black Labrador chew sticks together on the grass as my mum nearby sticks some bean stakes in the garden.]

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

☀️ Here are 3 research findings, 1 musical thought, and 1 question to consider this week (plus 🐶 pic).

3 IDEAS FROM RESEARCH

I. The clearest sign yet that Long Covid can be the immune system attacking itself

A big team at Yale and Mount Sinai (led by a personal hero of the Sunbeam, Akiko Iwasaki, and others) has shown that, in at least some of us, the body makes antibodies that turn on its own nerves and brain tissue.

They took antibodies from Long Covid patients and put them into mice - and the mice started showing the same kinds of symptoms, like new pain. This has been done before, but this was the first time that researchers have definitively been able to say ‘autoimmunity definitely causes the disease for a subset of patients’.

For this subset that means it’s not really about chasing a single virus any more. It’s auto-immune in a subset of people, autoantibodies > attack on nerve tissue > symptoms - and immune diseases are a field we already have tools for, like IVIG and ways of filtering the bad antibodies out.

So one of these days we’ll have a simple test that says “yours is the autoantibody type” - and then studies (or existing treatments) specifically for those people. Goodie!

Source: Yale News / Cell (28 May 2026)

II. A new “cure” effort, and a gut-sealing trial worth watching

At the PolyBio symposium this month, two things stood out (as highlighted by Cort’s excellent blog in Healthrising - he covers a lot more than the below). One is a new Long Covid Cure Initiative, with $10m behind it, built around sorting patients into proper subtypes first and then matching treatments to each group - this is such a theme these days in the research - find the subtypes and the rest follows.

The other is an early trial of a drug called larazotide. The gist is, a leaky gut lining lets viral bits spill into the blood and keep the immune system overwhelmed. Larazotide tightens those gut junctions back up. Early results in 107 people looked encouraging.

This one is also interesting because it’s about the tissues, not just the blood (which has been stealing the spotlight in the research of late).

Caveats: this is early, Phase 2a, small-ish, and “encouraging early results” is a long way from proven treatment.

Source: Health Rising - PolyBio 2026 Symposium (17 June 2026)

III. Hunting the exact targets behind our exhausted immune cells

A group of researchers (including Liisa Selin, who has lived with ME/CFS herself for decades) are trying to pin down the exact proteins that make our immune T-cells act up and exhaust themselves.

Yet another avenue for subtyping: if they can name the targets, they can start splitting us into real biological groups - e.g. a viral-persistence type and an autoimmune type - and each type points to a different treatment. Precision! This is not your grandma’s ME/CFS trials… It really feels like a whole new era.

Apparently several teams are now moving in the same direction, which is a good sign.

Source: Health Rising - T-cell targets (9 June 2026)

1 MUSICAL THOUGHT

In true long hauler style, I took quite a while to make this album of gentle ambient piano music with a friend of mine, in a very paced way over the last 3 years. Like the process itself, it’s very gentle and spacious, and I include it here incase you may find it relaxing.

If you prefer you can also listen on Bandcamp.

1 QUESTION FOR YOU

The state of ‘post viral chronic illness’ research is ever brighter, and yet…

When you read about research moving forward but no treatments yet, where do you sit between letting yourself hope, feeling frustrated, and also just carrying on with your life? Comments below :)

puppy p.s. (Making the most of some old bedding before it goes to the Salvation Army)

(alt text: Whisky the cream coloured toy poodle naps atop a box of old bedding sitting by the front door waiting to be donated)

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

☀️ Here are 3 of the more promising research findings from the last month, plus 1 thought and 1 question.

3 IDEAS FROM RESEARCH

I.

The biggest update this month is not just “more genetics”. It is genetics getting closer to treatment.

The UK government is backing SequenceME, a major project that will sequence the full (complete! total!) genomes of up to 6,000 people with ME/CFS. The aim is to find biological patterns that could lead to better diagnostics, clearer subtypes, and eventually targeted treatments.

This builds on the earlier DecodeME work, which found genetic signals linked to immune function, infection response, nervous system biology, and chronic pain.

That connects so neatly with the fascinating work done by PrecisionLife which HealthRising covered recently. One of the most interesting bits is PL’s focus on protective mechanisms. In plain English: they are not only asking “what makes people ill?” They are also asking “who are the people who have the ‘bad genes’ but didn’t get sick? What genes protected them? And what clues does that give for developing treatments?”

If a pathway seems to protect people, researchers can ask whether a drug could strengthen that pathway, mimic it, or reduce the opposite damaging process.

HealthRising notes that PrecisionLife has already used this kind of approach in another disease, ALS, where protective genetic clues are helping point towards possible treatment strategies. They have also identified candidate treatments for ME/CFS and Long Covid and are sharing them with research groups(!)

This is still early. But it is a better kind of early: not “we found a vague association”, but “we found pathways that might be testable”.

II.

A small controlled pilot suggests ear-based vagus nerve stimulation is tolerated for Long Covid, but while there were improvements, they were no better than the placebo group..

This is called transcutaneous auricular vagus nerve stimulation, or taVNS. It is a non-invasive form of stimulation delivered through the ear.

The promising part is that this was not just an anecdote. It was a randomised, sham-controlled pilot study, which means people were compared against a fake-treatment control.

Even though the results were not particularly promising, it is still great to see proper, high quality tests being done that help us understand better what works and what doesn’t. Of course, until we have proper subgroups it might be very hard to get positive results (it might help some but not others), unless trials are sufficiently large.

Source: PubMed

III.

A new Long Covid paper strengthens the case that PEM should be treated as central, not secondary.

The study found that post-exertional malaise frequency and severity were strongly linked to worse quality of life in Long Covid (mic drop).

That sounds obvious to patients, but it matters scientifically. It pushes back against the idea that Long Covid fatigue is just generic tiredness or deconditioning.

Why it matters:

• PEM-aware care should be built into Long Covid support

• Trials should measure PEM, not just broad fatigue (you’d be amazed how many haven’t in the past)

• Treatment plans that ignore PEM may miss the main driver of disability

This is one of those findings that feels less flashy than a drug trial, but it could improve both research design and patient care.

Source: Springer open-access paper

1 THOUGHT

How cool to think about genes as not just disease mechanisms but protective mechanisms - not just what makes us sick but what makes us healthy! It appeals to the optimist in me, as does the march towards more precision and targeted meds for the (still murky but emerging) different sub groups.

Source: All of the above

1 QUESTION FOR YOU

If you were a scientist (or if you are!): what would you want to study right now?

puppy p.s. Buds

[alt text: Whisky and Monty have moved in together and when not chewing each other’s ears are sunning themselves out back]

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

☀️ Here are 3 research findings, 2 thoughts, and 1 question to consider this week. Plus a movie recommendation and the usual cute puppy pic.

3 IDEAS FROM RESEARCH

I.
A recent trial found that fluvoxamine improved fatigue and quality of life in Long Covid, while metformin did not.

This stands out because fatigue is one of the hardest symptoms to treat across both Long Covid and ME/CFS. It is not a cure, and the study window was relatively short, but it is one of the clearest recent signals that a repurposed drug might meaningfully shift symptoms.

It also reinforces the idea that targeting brain-immune signalling pathways could be more useful than general “recovery” approaches.

Source: https://scholars.duke.edu/publication/1709678?

II.
The major NIH study program RECOVER is now testing baricitinib, an immune-modulating drug, for Long Covid.

This matters because it reflects a shift toward targeting specific biological mechanisms, not just symptom management. Baricitinib is already used in other inflammatory conditions, so if it works here, it could move relatively quickly into clinical use.

It is still early, but this is the kind of trial that could directly translate into treatment options.

Source: https://recovercovid.org/news/recover-tlc-opens-expanded-enrollment-reverse-lc-clinical-trial

III.
A new cerebrospinal fluid study in ME/CFS identified distinct protein patterns linked to neuroinflammation, autonomic dysfunction, and metabolism.

This is not a treatment yet, but it is a step toward objective biology. Instead of describing symptoms, researchers are starting to map what is actually happening in the nervous system.

Because Long Covid and ME/CFS overlap so much, findings like this could help define subtypes (rather than treating these illnesses as one big blurry category) and guide more targeted treatments over time.

Source: https://www.nature.com/articles/s41598-026-46965-1

2 THOUGHTS

I.
The most promising thread across all three is this: the field is slowly shifting from “managing symptoms” to testing specific mechanisms.

Drugs like fluvoxamine and baricitinib are not random guesses. They are being chosen based on hypotheses about immune signalling and inflammation.

That is a meaningful step toward treatments that are based on cause, not just coping.

II.
At the same time, biomarker work is catching up. The more clearly researchers can measure what is happening, the easier it becomes to match the right treatment to the right group.

This combination, better measurement plus targeted trials, is where real progress is likely to come from.

BONUS:

I watched a brilliant movie recently - I Swear. It’s the story of a guy with Tourette’s, struggling with developing the condition as a kid, facing constant barriers to living a normal life due to his mind and body working in a way outside his control… sound familiar? Although we are at the opposite end of the spectrum in terms of visible/invisible disabilities(!) it still really resonated with me. It’s a beautiful film showing the hardships but also the power of a kind helping hand, muddling through and making the best of a bad hand, and the sweetness of doing what you can to help others. I recommend! Oh and it’s funny :)

1 QUESTION FOR YOU

What’s something you care about now that you probably would have laughed at (or never thought of) pre-illness?

Pooch pic 📷 - yin yang

Alt text: Whisky the cream toy poodle and Monty the curl up together. (Whisky has a cone of shame on due to a broken nail- nothing too serious).

Wishing you a peaceful week

Tom and whisky

☀️ Here are 2 research findings, 1 thought, and 1 question to consider this week (plus 🐶 pic)

2 IDEAS FROM RESEARCH

I.

A £20 million project will read the full genetic code of ~18,000 people with ME/CFS and Long Covid - the largest ‘long-read’ genetic study for any disease.

Most genetic studies only look at the parts of DNA where differences are common. This one goes much further. It uses a newer technique called long-read sequencing that can spot rare changes, missing sections, and rearranged stretches that older methods miss entirely.

It matters because earlier work (the DecodeME study) already found eight genetic regions linked to ME. A smaller pilot suggested up to 40% of patients may have a genetic contributor to their illness. This project digs deeper into what’s driving things at the individual level.

What would be amazing: if specific genetic pathways show up, researchers can check whether existing drugs already target them. That could shorten the wait for treatments a LOT.

Phase 1 is funded. One to watch!

​II.

A new study from expert Carmen Scheibenbogen looked at immune complexes - clusters of antibodies and proteins - in people with ME/CFS and post-Covid illness. Both groups showed signs of vascular disruption, but through different routes.

• In ME/CFS, the disruption showed up in the tissue scaffolding between cells.

• In post-Covid ME/CFS, it showed up in blood clotting and clot regulation.

Different triggers, overlapping effects. That strengthens the case for microclots and blood vessel dysfunction as treatment targets - something already being explored in clinical work.

It also supports a topic dear to regular readers, and gaining steam - recognising subtypes. Knowing what’s the same and what’s different helps when designing treatments.

​1 THOUGHT

I’ve previously shared a children’s book from author Sara Robitaille – now she has a new one:

Families living with Long COVID, you are invisible no more. Two new children’s books, Long COVID Transformed My Mommy and Long COVID Transformed My Sister into a Turtle, offer gentle, kid‑friendly insight into what it’s like to be a parent or child with Long COVID. Very few children’s books talk about life with Long COVID, which is why Sara Robitaille, a mom in California living with disabling Long COVID, used her limited energy to create these books.

For millions of families, Long COVID has reshaped daily life. These two books use playful language and warm illustrations to help kids understand what their loved ones may be experiencing and to remind families they are not alone.

Order at dottieloni.com. Bateman Horne Center, Long COVID Kids, and Long COVID Families receive donations from the sale of these books.

Some pics from the books:

1 QUESTION FOR YOU

What’s one thing you wish you could try for your condition?

puppy p.s. Post swim chic

My folks have been looking after Whisky for a while – but that’s all changing as he moves into our new home, together with Monty the black lab - best pals reunited! Expect more duo pics in future!

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

☀️ Here are 3 research findings, 2 thoughts, and 1 question to consider this week (plus 🐶 pic and bonus 🐦‍⬛ pic).

3 IDEAS FROM RESEARCH

I.

Australian researchers are testing whether long Covid care can be delivered at scale …without sacrificing personalisation.

The Perceive-Outreach trial from the University of Tasmania’s Menzies Institute is recruiting a national cohort to test multidisciplinary remote rehabilitation.

Right now, most long Covid patients navigate their care alone, piecing together referrals, waiting lists, and specialist appointments. This trial is testing whether a structured, remote programme can do that coordinating for them.

What’s awesome is that this trial is built to reach patients wherever they are, including rural (Long Covid care has historically been fragmented and city-centric).

The cardiovascular focus is particularly notable. Heart damage in long Covid has been underappreciated, and this programme treats it as a core outcome.

II.

The problem with long Covid research has always been heterogeneity. Amatica thinks larger cohorts are the answer.

The non-profit Amatica is scaling up recruitment specifically to tackle one of the field’s most persistent frustrations: patients respond so differently that small studies keep producing contradictory results.

The logic is straightforward but important:

• small trials can’t reliably detect subgroups - people who share a specific biological pattern within the broader condition

• larger cohorts make it statistically possible to find those subsets

• once subsets are identified, targeted treatments become testable rather than theoretical

This is the same strategy that transformed oncology - moving from “cancer” as a single category toward specific subtypes with specific therapies. Long Covid research is now attempting the same shift.

Source: Healthrising article

III.

A new meta-analysis has done something the field urgently needed: taken stock of every pharmacological approach trialled for long Covid so far.

The preprint systematic review evaluated drug interventions across adult cohorts, with anticoagulants emerging as one of the more evidence-supported candidates - consistent with growing evidence that microclotting is central to long Covid in at least some patients.

Key points:

• several candidate agents show genuine promise, particularly around cardiovascular and thrombotic mechanisms

• the evidence base remains thin: most trials have been small, short, and inconsistently designed

• But TBH, what’s needed now is coordinated trial infrastructure - which fingers crossed, the big NIH RECOVER will finally start delivering on with lots of promising clinical trials happening now.

2 THOUGHTs

I.

Across these studies, one theme keeps emerging: subset identification. Whether it is immune mapping, ion channel dysfunction, or clot-related pathways, the field is slowly moving from “one condition, one explanation” to “multiple biological patterns under one label.” That shift could be the key to personalised treatment.

If immune profiling and cellular targets continue to replicate (which is seeming likely, as the field hones in!) we may be closer to objective testing and targeted subset treatment than we might think, after spending years in the doldrums of pacing/symptom-only management.

II.

I wanted to stop and appreciate two very different goals that pwME/LC can have.

→ One, to tirelessly keep trying things, to not give up hope, to seek for an answer.

→ And two, to stop and simply accept where you are with life.

I’m sure everyone does this differently. I don’t think there’s a right or a wrong (some may reject acceptance, or have given up hope).

I personally think hope and acceptance are the key to doing the best I can do as an individual with this condition. I am not someone who has tried the maximum treatment options, nor am I fully at peace with my situation. But I have certainly found many little ways to try and nurture these two qualities, which has helped a lot.

But both hope and acceptance are hard. Sometimes even out of reach. Wherever you are at, may you be able to give yourself even the smallest sliver of credit for having had to cultivate either of these traits.

1 QUESTION FOR YOU

How do you relate to hope and acceptance as a person with ME/LC/other chronic condition? Does it change?

puppy p.s. Post-beach hairstyle

Bonus pic: Kererū (New Zealand Wood Pigeon) stops for a drink

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

Apologies for the gap between the last Sunbeam - life and health got in the way. I’ve included an extra dog pic to make up for it at the end.

☀️ Here are 2 research findings, 2 thoughts, and 1 question to consider this week (plus 🐶 pic)

2 IDEAS FROM RESEARCH

I.

What I’m excited to see is a growing foundation of research that seems to explain the mechanics of ME and LC in a way that fits together. All the different findings can feel so disjointed → “blood clots! blood brain barrier! immune cell exhaustion!”.

In particular research talking about blood flow issues to the muscles really ties it together for me. There’s lots of nuance, but the gist [to my imperfect understanding] is that there are issues with getting oxygen to the muscles, which sets off a whole chain of other body responses that in turn make the problem worse and keep our bodies stuck in the loop.

(overload within the cells > mitochondria failure > inefficient and harmful backup mechanisms > reduced blood flow…)

What causes the blood flow issues? The things (receptors) that tell the blood vessels to open are overworked and exhausted, due to(?) immune activation or autoimmunity or viral remnants (or a combo of these).

For a more in depth explanation check out Healthrising’s recent articles:

→ Connecting the Dots: Open Medicine Foundation Researchers on the State of ME/CFS at the End of 2025 (a really great pulling together of different researchers’ work – so cool to see lots of overlapping findings!)

→ An Enigma No More? Is ME/CFS an Acquired Muscle Myopathy Disease? (deeper dive by Dr Wirth)

​II.

I’ve also been heartened to learn of the ‘JAK1 inhibitor clinical trial boom’ happening in Long Covid – there are several LC trials underway of these immunotherapies (the immune systems seem to be doing the initial triggering of the whole blood flow issues). Again, Healthrising has a good article (but detailed) on it here - aren’t we lucky to have Cort?

2 THOUGHTs

I.

I mentioned above about issues with blood flow getting to the muscles.

I’ve also found this a great way to explain the illness to others, and a great way to remind myself how using muscles makes me crash. I can use them a bit, but too much and it’s game over. This has helped me a lot in avoiding crashes.

II.

The last year and a bit, I’ve overdone it. Before then my health had improved from moderate to quite mild – I was able to do a lot, and I did. Now I’ve paid the price for overdoing it with fairly constant sickness. I think everyone with a post-viral illness like ME or LC is familiar with this boom bust…

So it’s time to stop booming! I decided that this year my resolution is to ‘do less’… on reflection that means ‘do less of what I feel like I ought to do’. Whether that is solve that extra work problem, or do that extra activity, or even check that news site.

I’m conscientious, brought up to do your best, so it’s been really helpful to have permission to take the foot off the pedal. Early days, but so far so good!

1 QUESTION FOR YOU

Would you like to share any goals or directions you’ve set regarding your health this month/season/year? Please feel free to leave a comment.

2x puppy p.s.

So close yet so far:

Bonus pic - cosiness ++

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 Want to support the Sunbeam? All profits go to my local charity ME/CFS Canterbury – they are amazing and offer specialist nurse services amongst other things) 🌟

☀️ Here are 3 research findings, 1 thought, and 1 question to consider this week (plus 🐶 pic)

3 IDEAS FROM RESEARCH

I.

A (promising) high-accuracy blood test for ME/CFS
UEA and Oxford Biodynamics published an epigenetic “3D genomics” signature that distinguished people with severe ME/CFS from healthy controls with ~92% sensitivity and ~98% specificity. An accurate biomarker test is great for validating peoples’ experiences, and drug companies require it before putting lots of money into drug dev.

Basically, it seems that getting ME makes certain genes fold in a certain signature way.

It was just a small study, and other researchers have expressed a need for bigger trials (including participants with milder conditions) before getting excited - but for me it was cool to see that the media got excited - very different times from 10 years ago when there was much less general interest!

Press release quote: This approach …has previously shown success in identifying disease-specific blood markers in highly complex inflammatory and neurological conditions such as fast ALS (amyotrophic lateral sclerosis), rheumatoid arthritis, and certain cancers. Source: News-Medical.net

+ Nature News more balanced opinion on the study.

​II.

A biological clue behind long-covid brain fog
Researchers have found higher levels of AMPA receptors in people with long covid who struggle with memory and concentration. This points to possible drug targets. It’s still early work with small groups, but it’s one of the clearest biological leads so far in the brain. It was also found to be a very strong diagnostic marker.
(Read the study on OUP Academic)

III.

More practical treatment studies inching forward in long-COVID trials
The big US RECOVER programme is moving into its next wave of interventional trials. They are way more practical than last time, and are testing various drugs that already have had small studies conducted or evidence in other conditions, including low-dose Naltrexone, GLP-1s, and stellate ganglion block (injection of anesthetic into the stellate ganglion nerves to improve circulation - has seemed to reset some peoples’ systems). Press writeup here (Chemical and Engineering News)

1 THOUGHT

How to help the long hauler thirst - Why oral rehydration solution (ORS) works better than plain water or electrolytes, and how to make it yourself

Many of us with ME or Long COVID find we get thirsty a lot. But drinking loads of plain water isn’t always the answer – your body often just flushes it straight out again. Adding a bit of sugar and salt helps your body actually hold on to the water.

This mix is called oral rehydration solution (ORS). It helps your body absorb water more effectively by using the sugar and salt to pull fluid into your bloodstream. You can make a simple DIY version at home: 500ml water, 3 teaspoons sugar, and ¼ teaspoon salt, sipped slowly over about an hour. If you have dextrose (a type of glucose), that’s even better, but ordinary sugar works just fine. You can also buy ORS solutions.

For many with ME or Long COVID, ORS can help ease symptoms like dizziness, fatigue, and that “crashed” feeling after standing. I really notice the difference, and feel more hydrated.

ORS isn’t the same as “electrolyte” drinks. Sports rehydration mixes are mainly for people who lose salts through heavy sweating. For those of us with ME or Long COVID, the issue is more about blood volume and hydration balance. the sugar + salt combo pulls sodium into the blood and water follows, so you actually absorb and keep the fluid instead of flushing it out.

As always, be careful and listen to what works for your body (especially if you have heart, kidney or blood-pressure problems, or take diuretics).

1 QUESTION FOR YOU

What is your experience with ORS, or electrolytes, or that everlasting long hauler thirstiness?

puppy p.s. Tuckered.

alt text: Whisky the toy poodle resting on his favourite arm chair after an outing.

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

☀️ Here are 2 research findings, 1 thought, and 1 question to consider this week (plus 🐶 pic).

This edition focuses on some new trials that use existing drugs.

2 IDEAS FROM RESEARCH

I.

A new clinical trial is testing an existing drug as a possible treatment for long covid.

This is cool because it’s an already FDA-approved drug, speeding up the development process.

ImmunityBio, a US-based immunotherapy company, has announced the start of a Phase 2 study to see if its drug ANKTIVA could help people with long covid.

ANKTIVA is an IL-15 agonist, which means it boosts the activity of key immune cells. These cells are important for fighting off lingering viral material in the body.

Dr Patrick Soon-Shiong, the company’s founder, explained that evidence shows viral proteins can linger in the gut months after infection. He said this means antiviral drugs alone may not be enough, and that strengthening the immune system could be a better approach. The hope is that ANKTIVA could help the body clear these remnants and ease long covid symptoms.

The new trial, called COVID-4.019-Long, will look mainly at whether ANKTIVA is safe when given as an injection under the skin. Researchers will also check how it affects immune cell counts and whether it can improve immune function.

👉 Find out more about the study here

​II.

Three new trials are testing ‘JAK inhibitors’ to calm the immune system

Three large clinical trials are underway to see if a type of drug called JAK inhibitors could help people with long covid by calming down immune system problems.

The drugs being tested are:

• baricitinib (Olumiant)

• upadacitinib (Rinvoq)

• abrocitinib (Cibinqo)

These medications are also already approved for autoimmune conditions like rheumatoid arthritis and eczema, but they are dangerous! They can cause very serious side effects since they suppress parts of the immune system.

Researchers believe long covid may partly be driven by the immune system staying stuck in an overactive state. JAK inhibitors target the JAK/STAT pathway, a key signalling route that controls inflammation.

One patient story shows how complicated this might be. Jen, who had ME for nearly two decades, tried Rinvoq after running out of options. At first it made her sicker, and she stopped the drug after two months. But weeks later, her immune markers normalised and she unexpectedly went into full remission. More than a year later, she remains well and is sharing her experience with researchers.

Now, three clinical trials are testing these drugs properly.

People with ME and long covid have already experimented with JAK inhibitors outside trials. Results have been mixed – some saw big improvements, even remission, while others felt worse or had to stop because of side effects like infections or dangerously low white blood cell counts – ie. they might only benefit some ‘subtypes’ of LC.

Unfortunately results won’t come for a few years - however it’s great to see more and more actual treatment studies! As one investigator put it, the fact that three separate groups have landed on the same class of drugs is a strong sign the research field is maturing.

Read more here (The Sick Times)

THOUGHT + QUESTION

While it’s exciting to see these new studies coming through, it’s also important to remember that the results will take a long time - that’s how good science works.

In practical terms, we’ve got to manage our symptoms and try to make things as good as they can be – be it through pacing better (being more forgiving of ourselves), trying different things for symptom management, or whatever works for you.

1 QUESTION FOR YOU

As a long hauler, do you personally try to balance hope with acceptance? What does that look like for you?

puppy p.s. Living their best lives

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

☀️ Here are 3 research findings, 2 thought, and 1 question to consider this week (plus 🐶 pic)

3 IDEAS FROM RESEARCH

I.

BioMapAI identifies new biological markers that help detect ME/CFS with 90% accuracy!

Very cool. The researchers worked with the Bateman Center, which is a top-notch ME research and care centre. They're also planning to make their data set publicly available in the hopes it could be used with Long Covid as well.

Good write up here.

​II.

Patrick Ussher (pwME) has written an incredible book called Understanding ME/CFS & Strategies for Healing.

In it he explains the leading ‘unifying hypothesis’ of ME – this is an evidence-based hypothesis put forward by leading researchers Wirth and Scheibenbogen. Patrick’s book is reviewed by Dr Wirth for accuracy ✅

It really helped me see how all the other research fit together as the hypothesis seeks to explain how the different biomechanics affect each other…. From low blood flow and low blood volume to unbalanced oxygen and sodium and calcium levels…. All fuelled by an overactive nervous system...

While it can still be a little overwhelming trying to visualize it all at once, that certainly has helped me have a better sense of how the pieces fit together. The book strikes a nice balance between taking something complicated and making it simpler without oversimplifying it. If you go to Patrick's website you'll also be able to find chapter 2 which covers the unifying hypothesis available for free.

Bonus: My ‘ME/CFS Unifying hypothesis explainer’ gpt

I decided to take the key research papers around the unifying hypothesis and make them into a custom ChatGPT bot that you can ask questions of. Take any answer with a strong grain of salt - AI can definitely make mistakes.

Try it here (free).

One use i’ve found is asking, ‘If I do thing x, will it help?’

or ‘I want to do thing x. according to the theory what could I do to make it more possible?’

III.

‘New research has found ME/CFS is partly caused by genetics, related to the immune and nervous system.’ This is the DecodeMe study, which found eight genetic differences in people with ME. It's the largest yet genetic study of ME.

Here's a breakdown with one of the researchers on RNZ.

‘It's being hailed as a milestone but it's not a definitive test - some of the eight differences are also often found in people without ME/CFS - so it can't yet be cleanly separated who's at risk and who isn't.’

2 THOUGHTS

I.

I was part of an interview with the ‘Listening to Families’ organisation a year or so back. They’ve just released it as a podcast. It was great to talk alongside Prof Warren Tate and School Counsellor Amanda Gillespie, and hear their experiences of having a child with ME/CFS.

Short blurb: Together, we answer families' questions about diagnosis, support, and moving forward.

II.

I made some piano music, just for fun one rainy winter evening:

1 QUESTION FOR YOU

Breathing is great for calming our overactive nervous systems. I love using the Breathe app (Mac or Android) for simple guided breathing… It allows you to set custom times for breathing in and out. Breathing in for 4 and out for 6 is one of my favs (it slows the heart)… also breathing in and out for 5.5sec each feels great.

My question: does any one else have a favourite in/out breathing count? (or other breathing exercise.

puppy p.s. workin’ hard or hardly workin’

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

☀️ Here are 3 research findings, 1 thought, and 1 question to consider this week (plus 🐶 pic)

3 IDEAS FROM RESEARCH

I.

Emeritus Professor (and fellow Kiwi) Warren Tate spoke to Radio New Zealand (19min) about his team’s work developing a new blood test to diagnose ME/CFS and long COVID- he says it’s close.

Warren’s team has compared blood samples from people with ME/CFS, long COVID, and healthy controls. They’re looking at “epigenetic” tags—tiny chemical switches on DNA that affect how genes work. Excitingly, their latest study found specific DNA changes that appear in all the people with ME/CFS and long COVID they tested, but not in healthy people. This means a reliable blood test could be possible in the near future. This is important for many reasons - validation, less disbelief from medics, and more $$ from drug companies for trials.

Their research paper just received positive feedback from expert reviewers, and they hope to do bigger studies to confirm the results. If a test becomes widely available, it could help people get diagnosed earlier and manage their condition better, possibly preventing it from becoming lifelong.

Research teams around the world, including in the UK, are working on similar blood tests. Warren’s group is now also looking at “cell-free DNA” in blood, which might give clues about changes in the brain and other organs, not just the immune system.

Message of hope: Warren remains hopeful: unlike some other brain diseases, ME/CFS and long COVID are not neurodegenerative, and people often retain their abilities if the symptoms can be treated or reversed (Warren’s daughter manages ME/CFS). He’s inspired by the resilience of patients and believes there is real hope for recovery and better lives ahead, thanks to new research.

I find Dr Tate to be a true hero! He’s well into his retirement years but he’s driven to keep going, keep learning and sharing. Thank you Warren!

​II.

A new study (published in Nature) has developed a much more accurate way to identify people with long COVID using electronic health records. By combining medical codes, symptoms, test results, and even doctors’ notes, the new LATCH algorithm can spot long COVID cases far better than older methods (it correctly identified about 75% of cases, compared to just 16% using the ‘U09.9’ LC code alone).

This is great because this helps researchers and healthcare providers get a clearer picture of who is affected.

It makes it easier to study long COVID, improve care, and develop better treatments in the future.

III.

Following on from my first item this week, the following research also hints that there may not be just one biomarker for ME/CFS, but several, depending on the patient subgroup. identifying these unique patterns could be the key to developing more personalised and effective treatments…

A recent study in Journal of Immunology has strengthened the case for ME/CFS being made up of different subgroups, rather than a single illness

→ By examining immune markers in the cerebrospinal fluid of patients, researchers found two clear clusters – one group showed much higher levels of neuroinflammatory markers, while the other did not. This could explain why some people respond to anti-inflammatory treatments while others don’t.

1 THOUGHT

A friend of mine, Mark, did an interesting experiment with ChatGPT recently. He asked it for suggestions of interesting ways to use it… it suggested they switch roles - it would pretend to be him, and he would pretend to be ChatGPT.

He was amused and gave it a try, and was amazed at how much it acted like him (a little scary i know!). It said “man i’m so stressed, not sure how i’m going to find time to manage my cafe, barista training, and i need to do this and that”… he replied (acting as ChatGPT) “which one feels the most overwhelming? I can offer some suggestions”.

They went back and forth - and at the end, he felt like he’d gone through some sort of ‘reverse-counselling’ - by giving ChatGPT-Mark advice, he got perspective and felt calmer.

1 QUESTION FOR YOU

I shared the above because it reminded me of something somewhat similar: how helpful it can be to treat yourself like you would a friend.

That has really helped me. It was cool seeing Mark do it in a new way with AI!

My question to you: do you treat yourself as kindly as you would treat a close friend? If not, why not? Are you not deserving of love too? (spoiler: i believe you are!)

puppy p.s. Nap o’clock

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

Special 50th edition announcement! I’m excited to share that all money from my lovely subscribers now goes to my local charity MECFS Canterbury!

Their fb page and support really helped me at my lowest. I ended up on the board (proud armchair board member!) and so I get to hear directly the great testimonials from people who use the service (part time specialised nurses, and other support).

So thank you paying subscribers –and don’t worry– I can def still afford to buy Whisky his treats! 🐶

And thank you everyone else for your readership, and lovely messages, they always make my day 🌻

Let’s get into it.

☀️ Here are some rapid fire research findings, 1 thought, and 1 question to consider this week (plus 🐶 pic).

RAPID FIRE IDEAS FROM RESEARCH

For the 50th edition I’m doing a rapid fire highlight of a bunch of recent research - separated by ME/CFS and Long COVID focus.

Don’t worry, if you came here for the fun, there’s an extra dose of silly in the second half of the newsletter.

quick summary (TL;DR)

Long COVID work is looking at both drug and non-drug approaches, with a handful of phase 2 trials up and running and emerging evidence for throat inflammation being a key player.

Recent ME/CFS studies are already testing new treatments in small trials and showing some relief, and there’s a growing push for better funding.

Both ME/CFS and Long COVID are having some big genetics studies coming through. These will shine the way forward for targeted treatments!

I.

long covid research advances

• FOXP4 gene emerges as key long COVID player in massive study
  A huge genetic deep-dive (6,450 cases, almost 1.1 million controls) found that a variant in the FOXP4 gene seems to set you up for long COVID—and it’s all about how well your lungs bounce back after infection. This means that lung-focused treatments could be top of the list for therapies. It’s a nudge to pivot some long COVID trials towards boosting epithelial recovery.
  Note that FOXP4 is the first replicated genetic risk factor for long COVID. Nature

• Pulling that thread: viral RNA persists in the throat but can be reduced with EAT
  In a small study Japanese researchers found persistent COVID virus lurking in the upper throat of long COVID patients over six months post-infection, driving local inflammation. A three-month course of weekly epipharyngeal abrasive therapy (swabbing with 1 % zinc chloride - ) markedly reduced viral RNA, dampened inflammation and repaired epithelium—providing a strong rationale for the larger, multi-centre trial now underway in Japan Scientific Reports

• phase 2 bezisterim trial targets neurological symptoms
  BioVie’s ADDRESS-LC study has dosed its first participants in a trial testing bezisterim—an insulin-sensitiser that crosses the blood–brain barrier—to address long COVID cognitive impairments and fatigue. Primary outcomes will assess cognitive function over an 84-day dosing period, with data anticipated mid-2026 Neurology live.

• shift towards personalised immunomodulators (match the right drug to the right person)
  Researchers are increasingly testing immunomodulatory drugs like baricitinib and bezisterim in trials such as REVERSE-LC and ADDRESS-LC, reflecting a move to tailor therapies based on individual immune profiles. Initial optimism centres on targeting neuroinflammation and metabolic dysfunction to improve quality of life The Washington Post.

​II.

me/cfs research highlights

• massive genetic study DecodeME nearing publication
  The ongoing DecodeME genome-wide association study, set to be the largest of its kind with 26,000+ participants, says:
  This week, the project team reached a significant milestone: we are into the final analysis stage which tests millions of DNA variants for their association to ME/CFS. Completion of the write-up and announcement of the results will follow as soon as possible.

  We are on target to deliver the results before the completion of the study in August and appreciate your continued patience and support.

• rapamycin phase 2 trial shows symptom relief
  A tiny phase 2 trial found that rapamycin helped people with ME/CFS feel less wiped out, sleep a bit better and stand up without nearly passing out. It’s not a cure, but it’s proof that tweaking cells’ energy machinery can move the needle HCPLive

• a repurposed drug hits the starting blocks
  The ReMEdi study is under way, testing a therapy already used in other fatigue syndromes. It’s randomised and placebo-controlled, so we’ll know soon whether it’s worth scaling up or filing under “nice idea, wrong disease.” Lindus Health.

• boosting cellular fuel is on everyone’s mind
  At an international ME/CFS meeting in Berlin, researchers shared preliminary data on oxaloacetate supplements, hyperbaric oxygen and rapamycin. The theory? Give your cells more fuel and they might actually use it. Early signals look intriguing, but larger trials are needed Health Rising (quick pre-summary and links).

III.

Overwhelmed by all that? Me too!

Check out the Spooniverse Directory for less overwhelm.

Creator Nita Jain:

Living with chronic illness often feels like having a second job — one where you're constantly searching for reliable information, support groups, and healthcare resources. We've all been there, bookmarking countless websites, taking screenshots, and trying to remember where we found that one helpful article.

A great, easy to use website (No account needed) that looks like this:

“The Spooniverse Directory is a searchable directory of healthcare resources, created by patients who understand the challenges of complex chronic health conditions. Think of it as your personal healthcare library, organizing everything from support groups to clinical trials in one easy-to-navigate space.”

1 THOUGHT

Great to see that the readers know who’s really pulling the strings around here!
(comments from last newsletter):

1 QUESTION FOR YOU

My question last time was, what is your long hauler spirit animal? I didn’t get many responses yet, so I thought I’d make it more fun.

If you’re keen for a bit of fun, check out the Spirit Animal Creator I made in ChatGPT - just answer 3 questions and it’ll visualise your spirit animal! (You’ll need to sign up for a free account if you don’t have one).

Here’s mine:

What’s yours?

puppy p.s. New best bud… Introducing Monty!

Wishing you a peaceful week,

Tom and Whisky (and Monty)

☺️

This newsletter is and always will be free.

🌟 If you would like to support my local charity ME/CFS Canterbury, you can by upgrading to paid (100% of donations go to them - they are amazing and offer specialist nurse services amongst other things) 🌟

My sincere apologies, I've been painfully busy the last couple of months, but now I'm back to normality.

To help you forgive my sins, I've included extra research findings as well as a special announcement from a reader! And of course the pooch pic!

☀️ Here are 5 research findings, 1 thought, and 1 question to consider this week (plus 🐶 pic)

5 IDEAS FROM RESEARCH

I.

This excellent blog article by HealthRising breaks down an exciting new update in immune science in general: using AI, researchers decoded complex patterns in immune cells (T and B cells) and could often tell who had autoimmune diseases, diabetes, or even a recent flu jab. As the blog says:

• When applied to a single disease, the authors stated these techniques can pluck out subsets and track treatment effectiveness.

• That’s where diseases like ME/CFS and long COVID come in. [Expert] Eric Topol said that this technique was perfect for deciphering mysterious, heterogeneous, immune-based diseases like ME/CFS, long COVID and post-treatment Lyme syndrome.

So this is the “immunome”- a way to easily track all immune activity. The researchers say it's moving fast and could become affordable. Let’s see what it enables!!

​II.

A Nature study revealed some interesting brain chemical imbalances in ME/CFS—and how they change after exercise.

No surprise, exercise made things worse for the ME/CFS group –their levels of many chemicals dropped, while healthy people’s levels rose.

This could help explain why rest doesn’t help after exertion in ME/CFS.

One key takeaway: the way the brain processes energy in ME/CFS looks different from healthy people—and different from earlier studies showing a “low-energy” state in the blood. The brain might be running hot in some ways and cold in others.

III.

Blood-based tests for ME/CFS may be getting closer to reality

There’s still no simple blood test for diagnosing ME/CFS — but this new review pulls together promising research that might change that:

• abnormal mitochondrial function, including issues with producing ATP (the cell’s main energy source), showed up in several studies. one approach using three different markers hit almost 100% accuracy — though it’s still early days.

• metabolomic profiling (which maps chemical fingerprints in the blood) has reached diagnostic accuracy as high as 98% in some machine learning models.

• raman spectroscopy, a quick laser-based method, showed it could sort people with mild, moderate, and severe ME/CFS using just a small blood sample.

the big challenge now is proving these tests are specific to ME/CFS and not just picking up on general fatigue or inflammation seen in other illnesses. but researchers are hopeful — especially as better diagnostics could mean earlier treatment and less misdiagnosis.

for long haulers, this review hopefully indicates that objective testing might not be that far off. the science is moving in the right direction!

IV.

a new(ish) theory says long covid and ME/CFS might come from a ‘traffic light’ in your cells getting ‘stuck on green’.

the traffic light is called mTORC1, and it helps control how your cells use energy, grow, and recover.

normally, it switches on and off to keep things balanced.
but if it’s stuck “on” all the time, your cells can’t rest or repair properly.
that could explain why people feel exhausted, foggy, and never seem to bounce back after doing even small things.

this idea ties together a lot of what we already know—like problems with energy, the immune system, and even reactivated viruses.

and here’s the exciting part:
if this “stuck traffic light” theory is right, there are already drugs that might help reset it.

still early days, but it gives researchers a clearer target—and that’s a big deal.

source: mTORC1 syndrome (TorS): unifying paradigm for PASC, ME/CFS and PAIS

V.

another possible reason your body can’t switch off after a virus? trained immunity.

a separate mini-review raised a fascinating (possibly related?) angle: ‘trained immunity’.

it’s not the usual kind of immune memory with antibodies. trained immunity is when your innate immune system—the part that reacts first—stays on high alert, even after the infection is gone.

some early research in long covid and ME/CFS suggests this could be part of the problem. instead of healing, the body keeps sounding the alarm.

it’s still a working theory, but it fits with what many people experience: feeling like they’re always running on empty, even after doing almost nothing.

Special announcement ❤️

A Sunbeam reader, Sara, got in touch with me about a beautiful book that she has published recently. Read on…

Announcing the release of Long Covid Transformed My Mommy a new children’s book written by Sara Robitaille, a mom living with disabling long covid.

I am a person living with disabling long covid and wrote this book over the last 2 years little by little. For the millions of parents all over the world who have been physically and mentally changed by disabling long covid, their love for their children remains unchanged. In playful descriptions and whimsical illustrations this book helps children understand what their parent with long covid is experiencing. It also lets children and parents know they are not alone during this difficult time for their family.
All my profit from the sale of the first printing will be donated to Bateman Horne Center, a non-profit working to educate, treat and research treatments for people living with long covid and other post viral illnesses. Please share and help me get the word out about this new resource!”

Sara shared with me:

“If I find an audience for this one I have already started on a version about being a kid with a long covid that I hope to publish next. There are so few books available for kids on long covid that I think these can help children and families feel validated, seen and understood and help other readers better understand that long covid is real and worthy of attention, research and community support.”

Keen to buy the book? Purchase here! (all profits go to Bateman Horne Centre)

1 QUESTION FOR YOU

What is your long hauler spirit animal version of yourself? What would the caption be?

Last time’s question: What are some digital apps that make your life easier?

Thanks dear readers for your responses below…

Jo:

I’m loving using the self care app - Finch-

And I find the Bearable app really good for tracking symptoms, impact of medication and other factors like what I am eating, how much sleep etc

Andrew:

Simple meditation timer that I use to take a 5min break several times a day:

Apple Shortcut that quickly plays relaxing music on Spotify - I like having it on my home screen so I can get it quickly when I’m stressed:

This is an app for gut hypnotherapy. I’m a sciencey person and always thought hypnotherapy was a bit out there, but the evidence has really started stacking up. For people with IBS, this app is as effective as following the full FODMAP diet. I don’t technically have IBS, but I find when I’m stressed (a lot of the time with long covid!) that I get tense in my stomach and it affects my bowel habits, and I find this app incredibly helpful. It’s not cheap AU$200, so more like the cost of seeing a specialist doctor. I’ve found it good enough that I still recommend it to anyone with any gastrointestinal symptoms who has the budget

Jobi:

I use Insight Timer to search for guided meditations, Visible app to track symptoms, and Find What Feels Good which has a lot of yoga but most importantly makes searching for restorative, brief, and low-to-the-ground guided sessions

puppy p.s. Beach time - Whisky’s happy place!

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free. If you would like to support my writing, you can by upgrading to paid.

☀️ Here are 2 research findings, 1 thought, and 1 question to consider this week (plus 🐶 pic).

2 IDEAS FROM RESEARCH

I.

New study identifies five subtypes of long COVID

A new study from the National Institutes of Health’s RECOVER Initiative has identified five distinct subtypes of long COVID. By categorising symptoms into these groups, hopefully researchers can pinpoint their experiments better and doctors can give more targeted advice more easily.

Why this matters

Long COVID has been difficult to define and treat, largely because it affects people in different ways. By identifying patterns among 14,000 patients—plus an additional 4,000 in a 2024 update—scientists have grouped symptoms into five categories. This could help doctors provide more tailored care and, in the long run, lead to more targeted treatments.

The five subtypes of long COVID

Each subtype includes a range of symptoms, but they vary in severity and impact on daily life.

Subtype 1: Milder symptoms, mostly affecting taste and smell

• 100% reported changes in taste or smell.

• Fatigue (66%) and postexertional malaise (53%) were common but less severe than in other subtypes.

Subtype 2: More severe fatigue and chronic cough

• Postexertional malaise (94%) and fatigue (81%) were dominant symptoms.

• 100% had a chronic cough.

• Symptoms in this group overlap with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Subtype 3: Brain fog and dizziness take over

• 100% reported brain fog, making concentration and multitasking difficult.

• Fatigue (92%) and postexertional soreness (82%) were also common.

• Some symptoms resemble postural orthostatic tachycardia syndrome (POTS), a condition affecting circulation.

Subtype 4: Palpitations and gut issues

• Palpitations (92%) and dizziness (71%) were key symptoms.

• 60% reported gastrointestinal issues, and 36% experienced fever, sweats, or chills.

Subtype 5: The most severe, affecting multiple organs

• Nearly all reported shortness of breath (99%), postexertional soreness (98%), and dizziness (94%).

• 80% experienced gastrointestinal problems and 78% had muscle weakness.

• This group had a higher proportion of unvaccinated individuals and people infected before Omicron, suggesting a potential link to more severe COVID variants like Delta.

How this helps patients

Doctors can now use this five-type index to identify which group a patient falls into and offer more specific care. While long COVID treatments aren’t doing much for many of us yet (understatement!), recognising symptom patterns is a step toward better management—and surely, better treatments.

​II.

Interesting! Study finds larger hippocampus in Long COVID and ME/CFS patients

New research from Griffith University has found striking brain similarities in people with Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), particularly a larger-than-normal hippocampus—a brain region linked to memory and thinking skills.

What’s causing the change?

The researchers suggest that a larger hippocampus could be the result of neurogenesis (new neuron growth) or possibly a lingering virus affecting the brain. This unexpected brain growth may be due to inflammation or immune system activation rather than the usual brain shrinkage seen in neurodegenerative diseases. Researchers believe ongoing immune activity is disrupting brain function, causing memory problems and brain fog.

Why this matters

This study adds to growing evidence that Long COVID and ME/CFS share biological similarities, particularly in how they affect the brain. MRI scans could become a new biomarker for long COVID and ME/CFS, as hippocampal changes were found in most affected patients. It could also pave the way for future research into treatments targeting cognitive issues in both conditions.

1 THOUGHT

I.

Here are some phone apps that make my life better. I’ve mentioned some before .. these are SO good for helping calm my system.

Breathe (iphone) (android) - a breathing app WITHOUT annoying sounds, just a really relaxing voice!

Yoga Nidra (iphone) - wonderful, lying guided meditation, with varying lengths

7 Min Chi (iphone/android) - this got me into Qigong, and it really did wonders for me. WARNING: if you experience PEM very easily, then this might be too much. If you have mild ME/CFS, this might be for you. (standing, moving arms).

OneSec (iphone/android) - stops you from opening phone apps so easily… great to break that addictive impulse…

SuperWhisper (for iphone - also for mac desktop) - this one uses AI to transcribe really well what you say, then paste into somewhere else. You can also customise it to automatically format what you say, into an email, or a note, or other things. Free with some paid features.

Bonus mentions: textsniper for mac - allows you to copy text from anywhere like you’re taking a screenshot – and intermission for mac, reminds you to have regular breaks when using computer!

1 QUESTION FOR YOU

What are some digital apps that make your life easier?

puppy p.s. Flashback to a younger Whisky!

(Whisky the cream toy poodle holds a skinned half-tennis ball in his mouth, stares at camera)

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free. If you would like to support my writing, you can by upgrading to paid.

☀️ Here are 3 research findings and a question to consider this week (plus 🐶 pic)

3 IDEAS FROM RESEARCH

I.

An Exeter-based research firm, Attomarker, has developed a finger-prick blood test that could help confirm Long COVID in patients – a potential game-changer for diagnosis and treatment.

🔹 A new way to diagnose – The test sorts Long COVID patients into three groups based on their immune response.
🔹 What the test found – 60% of patients showed weak antibody responses, 15% had an overactive immune reaction, and 25% had unclear results.
🔹 Why it matters – This provides hope for targeted treatments, and more likelihood that pharma companies will invest big bucks, since drug development is much easier with good diagnostic tests (by knowing that people in different subtypes are getting what they need).
🔹 Caution before rollout – COVID expert Prof David Strain says, "Just because there is a test, it doesn’t mean it should be rolled out across the board. This needs a bigger trial… The right way forward is to collect around 300 patients, identify which cohort they fit into, treat them, and see if they get better"

If proven at scale, this could be a major step forward in tackling Long COVID – but more research is needed.

Source: BBC

​II.

A new study builds on evidence that SARS-CoV-2 spike proteins can linger in the brain and skull bone marrow for years, possibly driving chronic inflammation.

🔹 Spike protein persistence – Found in the meninges and skull marrow up to four years post-infection.
🔹 AI-powered discovery – Cutting-edge imaging technology helped uncover these hidden spike proteins, showing their unexpected distribution.
🔹 Vaccination impact – mRNA vaccines reduce spike protein accumulation in the brain by about 50%, but don’t eliminate the risk entirely.
🔹 Potential for new treatments – Targeting lingering spike proteins could open doors for diagnosing and treating Long COVID-related neurological damage.

Source: Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19

III.

Normally this blog focuses on positive news, however I also enjoy the power of a good vent! So thank you NPR writers…

Frustration mounts as US federal research on Long COVID still lacks treatments

🔹 Four years in, no FDA-approved treatments – “It’s unconscionable that more than four years since this began, we still don’t have one FDA-approved drug,” says Meighan Stone of the Long COVID Campaign.

🔹 $1.15 billion spent, but where are the results? – Despite the NIH’s RECOVER initiative, some researchers believe the program lacks “clarity of vision and clarity of purpose.” Dr. Ziyad Al-Aly says, “What [RECOVER] lacks, really, is clarity of vision and clarity of purpose.”

🔹 Patients feel gaslit – Long COVID patients often struggle with doctors dismissing their symptoms. Chimére L. Sweeney of the Black Long COVID Experience says, “You’re at the whim of somebody who may not even understand the spectrum of Long COVID.”

🔹 NIH defends the slow pace – “Good science takes time,” says NYU’s Dr. Leora Horwitz, pointing out that the condition affects nearly every organ system, making it difficult to study.

🔹 Not enough focus on treatments – “Only 15% of the budget is for clinical studies. That is a failure in itself—a failure of having the right priorities,” says Dr. Ezekiel J. Emanuel.

🔹 Insurance battles make it worse – With no approved treatments, Long COVID patients must rely on off-label drugs, often paying out of pocket. Hyperbaric oxygen therapy, for example, can cost up to $8,000.

🔹 A glimmer of hope? – NIH recently requested proposals for new treatment research, but patients remain skeptical. “The name’s a little cruel and misleading,” says JD Davids of Long COVID Justice, referring to the RECOVER initiative.

Call me naive, but I have faith we’ll get there. In the meantime, I’ll take satisfaction like the Germans do in a good grumble!

Source: NPR

1 QUESTION FOR YOU

What gives you the most satisfaction to vent about?

puppy p.s. Whisky stares mischievously up at a beautiful kererū / NZ wood pigeon safely out of reach in a silver birch

This was the first time a kererū ever landed in this tree… you can admire their beauty up close in this youtube vid

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free. If you would like to support my writing, you can by upgrading to paid.

☀️ Here are 3 research findings and 1 thought for you (plus 🐶 pic). Here’s to a better year ahead!

3 IDEAS FROM RESEARCH

I.

Last time I posted a Medscape article on ‘promising treatments’ for long haulers. Understandably, there was a whole lot of disappointed, angry and frustrated comments that the treatments it highlighted were nothing new, and nothing that effective. There were a lot of comments that antivirals and the like are what we need based on the emerging research.

I agree! I really do!

So it was very exciting to hear that top researcher Nancy Klimas has just received FDA approval for a fully funded randomized controlled trial on the efficacy of using a monoclonal antibody to treat Long COVID. This is using an existing antiviral combo (developed by Astra Zeneca to help with acute COVID).

The reason for the trial is a case study she coauthored with a physician, who had treated 3 long haulers who had come in with acute COVID, and by chance found that the treatment also put their LC into remission… in about a week! Amazing! Since publishing the case study, the physician has had improvements from ~19 out of 21 other patients, according to Nancy Klimas in this podcast interview.

She hasn’t published any press updates about this yet, but from listening to the podcast interview I am 99% certain it’s not fake news! (or AI has become very good at impersonating Nancy!). In the podcast she says she is beginning the study early next year.

That means it will take a while for us to hear anything, but it is a very promising strand of research, and because it is using an existing antiviral that speeds things up.

If you’re interested, here’s the case study that prompted the study.

​II.

FYI here’s a sum up of why antivirals may help based on recent studies…

While there remains no single study that confirms that persistent virus is the cause of long COVID, collectively several recent key papers make a compelling case.

• Long-Lasting Virus Presence Increases Long COVID Risk
  People with mild COVID-19 who continue to have virus particles in their body for a long time are more likely to develop long COVID symptoms.

• Virus Can Keep Replicating in the Body
  Studies have found that the virus can still make copies of itself in the blood even years after the initial infection.

• Virus Found in Various Body Tissues
  Research shows that the virus is present in multiple parts of the body, like different tissues and blood, months after getting sick. Those with ongoing virus presence are at higher risk for long COVID.

• Gut May Harbor the Virus
  The digestive system might be a key area where the virus hides, leading to long-term health issues.

Challenges and the Need for Action

• Hard to Detect Live Virus in Hidden Areas While it's clear the virus can stay in the body, finding live virus in these hidden spots is difficult, making it hard to prove for sure.

• Urgent Need for Treatment Research Even with these challenges, scientists believe the evidence is strong enough to push for more research into treatments that target the lingering virus.

Source: The Conversation

III.

Here’s a summary of a new preprint article that surveyed ~4000 Long Covid and ME/CFS patients regarding 140+ different medications, supplements, and non-drug interventions.

1. Patient Subgroups with Distinct Needs

• Four clusters were identified: (1) Multisystemic symptoms, (2) POTS-dominant, (3) Cognitive and sleep dysfunction with pain, and (4) Milder symptomatology.

• Most Beneficial Treatments Identified

• Top-rated treatments included pacing (75.2% Net Assessment Score, NAS), fluids/electrolytes (68.6%), and low-dose naltrexone (49.4%). These were effective across all patient subgroups.

• Fluids/electrolytes most frequently helped POTS (71.7%), and to a lesser extent, fatigue or low energy (43.2%), PEM (33.2%), and brain fog (36.5%).

"Pacing and fluids/electrolytes demonstrated significantly higher perceived benefit over the reference treatment."

The below picture shows the effect of different treatments. The more orange/yellow, the more people reported it helped them. And the more blue, the more people said it harmed them.

3. Treatment Perceptions Across Conditions

• It didn’t matter much whether you had LC or ME/CFS – patients reported similar responses to treatments, with a high correlation (R² = 0.68) between ME/CFS and Long COVID outcomes.

"This study underscores the symptomatic and therapeutic similarities between ME/CFS and Long COVID."

These self-reported surveys aren’t as accurate necessarily as a full clinical trial but they are still really great if you take them with a grain of salt. Plus, with Stanford’s Ron Davis as co-author, it’s as good as it gets.

Credit to LONGCOVIDPHARMD, one of the authors, who also writes an excellent substack where she breaks down her community analyses.

1 THOUGHT

A friend of mine recently told me about how much better he’s been since doing the Lightning Process. Like many in our community, I am very skeptical of it and similar programmes, because of their ability to do harm. But I think they probably do help some people, and so I dug a little deeper and wrote a short piece on what aspects from the LP resonate with me, as well as what I dislike.

In case you don’t know, from what I understand the Lightning Process is a programme that combines techniques from neuro-linguistic programming, life coaching, and mind-body training to help individuals reframe thoughts and behaviours to manage chronic illness. It has received flack for causing many Long Haulers to permanently worsen, since it encourages a mindset of extreme positive thinking.

Full disclaimer: I haven’t taken a LP course, and I’m not really planning to. But when I researched online what it promotes, I realised that I do some of this stuff anyway:

• I’m a big fan of actively helping my body relax, and moving my body very gently and intentionally (yoga nidra, tai chi/qi gong, or body scanning)

• I believe that reframing the negative has mentally helped me cope, and increased my ability to tolerate stress and hardship

BUT I hate the idea of pressure, or that my getting better is because I failed to think positively enough, or do these practices ‘the right way’. That pressure can come from others (‘why aren’t you helping yourself?’ or ‘why aren’t you trying harder?’) or from yourself. With all that context in mind, here’s my piece:

Learning from the Lightning Process: Extracting the Positives Without the Pressure and Guilt

For those with ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome), the Lightning Process can be a polarising topic. While its advocates highlight the benefits of mindset shifts and mind-body techniques, others feel burdened by the implicit suggestion that recovery is within their full control—a notion that can feel guilt-inducing or dismissive of the illness’s complexity. Here’s a reframed approach for those skeptical of the Lightning Process but curious about its practical takeaways.

1. Embrace Techniques, Not Guarantees

The techniques promoted by the Lightning Process—such as cognitive reframing, relaxation exercises, and body awareness—are tools that may support recovery but are far from a guarantee. Every person’s journey with ME/CFS is unique, and external factors like support systems, stress levels, and overall health play significant roles. Letting go of expectations for quick or definitive results can help you use these tools as part of a long-term strategy without unnecessary pressure.

2. Recovery Is a Long Game

Improvement can take time, and that’s okay. For many, progress unfolds over months or even years of consistent effort. For example, you might find benefits from relaxation techniques like yoga nidra, tai chi, or body scanning—practices that promote calm and resilience but often work subtly and gradually. Your pace and progress are entirely valid, even if it feels slow.

3. Learn Without Overdoing It

A key barrier to the Lightning Process for some is its intensive course format. For those with ME/CFS, the idea of attending a demanding training programme can feel overwhelming, both physically and emotionally. The good news? You don’t need to attend a course to learn valuable techniques. Many of the principles align with broader holistic practices like meditation, gentle movement, and positive psychology, which you can explore at your own pace, in your own environment, without fear of a crash.

4. Focus on What Works for You

Not every technique will resonate, and that’s fine. The aim is to discover what supports your well-being (if any) and stick with it. For some, this might mean affirmations or visualisations to encourage positive thinking. For others, it could be practising deep breathing, tai chi, or spending time in a supportive, low-stress environment. Your health toolkit should feel empowering, not like an obligation or a test of willpower.

5. Remove the Pressure to “Fix” Yourself

Perhaps the most important takeaway is to let go of any sense of blame. ME/CFS is a complex and poorly understood condition, and while practices like these may help you feel better, they are not a cure (in my experience anyway – if it works for you, great!). Adopting a compassionate mindset towards yourself can help you focus on what feels good, rather than what you think you “should” be doing.

As someone who hasn’t done the LP, but is a firm advocate of active rest, reframing (when appropriate and possible), acceptance and self-compassion, I hope this is useful. If I have misrepresented the LP, my bad! –but also, why not share its’ practices freely rather than having to do a paid course? :)

1 QUESTION FOR YOU

What experiences/stories of the Lightning Process (or similar) can you share?

puppy p.s. Lightning Puppy

[alt: Whisky the cream toy poodle, mid-charge on the beach with a feather in his mouth and ears flapping]

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free. If you would like to support my writing, you can by upgrading to paid.

☀️ Here are 3 research findings, and 1 thought to consider this week (plus 🐶 pic)

3 IDEAS FROM RESEARCH

I.

Here’s a short simple review by Medscape called “New Data: The Most Promising Treatments for Long COVID”… The treatments highlighted include LDN, SSRIs and antidepressants, Modafinil, Metformin and antihistamines.

Here’s the original short article on Medscape (requires signing up for a free account)

And my quick summary of each:

Low-Dose Naltrexone (LDN)

• Original Use: An anti-inflammatory agent approved for treating alcohol and opioid dependence.

• Research Insights: "Low-dose naltrexone was associated with improvement of several clinical symptoms related to long COVID such as fatigue, poor sleep quality, brain fog, post-exertional malaise, and headache." (Medscape)

Selective Serotonin Reuptake Inhibitors (SSRIs)

• Original Use: Antidepressants that increase serotonin levels in the brain.

• Research Insights: Research from the University of Pennsylvania indicates that reduced serotonin levels may contribute to long COVID symptoms, suggesting SSRIs could be beneficial.
  "A study published in the November 2023 issue of the journal Scientific Reports found that SSRIs led to a ‘considerable reduction of symptoms,’ especially brain fog, fatigue, sensory overload, and overall improved functioning." (Medscape)

Modafinil

• Original Use: A medication used to treat narcolepsy and promote wakefulness.

• Research Insights:
  Has been shown effective for the treatment of fatigue and neurocognitive deficits caused by long COVID, said Viswanathan. She said that it’s another medication that she’s found useful for a number of her patients… [but has] interactions with other medications. (Medscape)

Metformin

• Original Use: A common diabetes medication with anti-inflammatory properties.

• Research Insights: A study in The BMJ reported that metformin reduced the incidence of long COVID when taken during the acute phase of infection.
  "Metformin seemed to reduce instances of long COVID in patients who took it after being diagnosed with acute COVID. It seems less effective in patients who already have long COVID." (Medscape)

Antihistamines

• Original Use: Medications that block histamine receptors to reduce allergic reactions.

• Research Insights: Some patients report symptom improvement with antihistamines, potentially due to their effect on mast cell activity.

• “For some patients, these can be a lifesaver,” said David Putrino, a national leader in the treatment of long COVID.
  "Research has shown that long COVID symptoms improved in 29% of patients with long COVID." (Medscape)

⚠️ Putrino cautions patients toward taking these and other medications haphazardly without fully understanding that all treatments have risks, especially if you’re taking a number of them.

“Often patients are told that there’s no risk to trying something, but physicians should be counseling their patients and reminding them that there is a risk that includes medication sensitivities and medication interactions.”

​II.

A Healthrising interview with Dr Avindra Nath gave an accessible breakdown of the largest yet study of ME/CFS, published earlier this year.

Nath:

We believe that the primary defect is in the maturation of B cells which leads to immune exhaustion and activation of innate immune responses…

We did not find any structural abnormalities but multiple functional or network abnormalities, which gives hope that the disease is treatable and possibly reversible.

[The study] convincingly demonstrated the biological basis of the disease that cannot be explained by deconditioning and psychological factors and identified several novel targets for modifying the course of the disease.

Other key findings highlight significant differences between men and women in immune responses.

The NIH study (“Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome”) lasted eight years, involved more than 70 authors from 15 countries, and was published in Nature Communications in February this year.

III.

“A new AI tool could identify more people suffering from long COVID from their health records” according to this article about a new research tool.

“Our AI tool could turn a foggy diagnostic process into something sharp and focused, giving clinicians the power to make sense of a challenging condition,” said senior author Hossein Estiri, PhD (at Mass General Brigham). “With this work, we may finally be able to see long COVID for what it truly is—and more importantly, how to treat it.”

“Physicians are often faced with having to wade through a tangled web of symptoms and medical histories, unsure of which threads to pull, while balancing busy caseloads. Having a tool powered by AI that can methodically do it for them could be a game-changer,” said Alaleh Azhir, MD, the co-lead author.

News article: Technology Networks

Link to study, published in Med

1 THOUGHT

A philosophical one for you: is strength measured by what we achieve, or by how we endure? Who’s stronger, you or the person who’s winning?

puppy p.s., Sweet Pea!

[whisky the toy poodle is curled up cosy on a lazy boy next to one of his humans]

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free. If you would like to support my writing, you can by upgrading to paid.

☀️ Here are 4 research findings, 1 thought, and 1 question to consider this week (plus 🐶 pic)

4 IDEAS FROM RESEARCH

I.

Researchers at Griffith University have focused on "immune exhaustion" as a shared yet distinct feature in LC and ME/CFS.

This is the first analysis of immune gene expression in both ME/CFS and long COVID patients at the same time, spotlighting specific immune pathways and markers that could differentiate these conditions.

Basically, the immune system in people with ME/CFS and long COVID seems to get "tired" or lose some of its ability to work properly over time. This could explain the long-lasting symptoms people experience, like fatigue and brain fog.

​II.

I really enjoyed listening to this podcast on how AI is changing how we do drug discovery.

The key takeaway is that we usually try to reduce very complex systems and problems into things we can understand, whereas AI doesn’t need to, and so has a much better chance at actually solving things and inventing new drugs.

This also removes the attachment that researchers might get to individual ideas, which might actually lead nowhere (happens 9/10 times in drug discovery), since the AI is able to test lots in a simulated environment at first (dry lab), which brings up totally unexpected treatment possibilities that human researchers have not looked at.

It’s early days and it will take a while but this is undoubtably the start of a new era for drug discovery…

In this episode of NVIDIA’s AI Podcast, host Noah Kravitz speaks with Chris Gibson, cofounder and CEO of Recursion, about how the company uses AI and machine learning to accelerate drug discovery and development at scale. Tune in to hear Gibson discuss how AI is transforming the biopharmaceutical industry by increasing efficiency and lowering discovery costs.

III.

Scientists at the University of Alberta have discovered two proteins that could help in identifying and treating long COVID. These findings help pinpoint what’s happening on a biological level in long COVID. If the proteins (galectin-9 and artemin) are playing a major role, then treatments could be developed to target and reduce these proteins.

Galectin-9 is linked to inflammation and brain fog.

Here’s how it works: when your immune system is stressed (for instance, from a COVID-19 infection), certain immune cells called neutrophils (a common type of white blood cell) get overworked and start releasing extra galectin-9. This protein ramps up inflammation in your body and is thought to worsen brain fog and similar cognitive issues. Essentially, galectin-9 might explain why you feel like you’re “in a fog” and struggle with clear thinking or memory.

Artemin is tied to severe pain and cognitive problems.

Researchers noticed that people with long COVID often have a lot of immature red blood cells circulating in their blood—something that usually only happens in bone marrow, where blood cells are made. These immature cells seem to raise levels of artemin, which in turn may worsen pain and contribute to mental fatigue or difficulty concentrating. Additionally, these immature red blood cells can suppress the immune system, potentially making it harder for your body to fully recover.

The researchers also challenged the theory that lingering traces of the virus itself cause long COVID. The team found no signs of the virus in the blood of long COVID patients a year after their infection. This points instead to chronic inflammation as a possible cause, fueled by proteins like galectin-9 and artemin.

IV.

This study published in Nature suggests that treating COVID-19 early with on nirmatrelvir-ritonavir antivirals reduces the chance of developing LC, although more study is needed to figure out just how effective they are.

1 THOUGHT

I.

If you are very noise sensitive, the Soundprint app is a great way of finding out where quiet cafes or other public places are. It’s crowdsourced, people report how noisy a place is for the benefit of others. Love it

1 QUESTION FOR YOU

A friend of mine, Makaira, is really good at treating himself when he needs it. What are your favourite bucket-filling treats? (doesn’t have to be edible)

puppy p.s. The Original Whisky!

Meet Archie, who is the same breed as Whisky (toy poodle x lowchen cross) and inspired us to get the same type of pooch due to his lovely companionable nature.

[alt: An older man sits at a table with a small grey dog resting its head in front of him, set against a scenic outdoor backdrop.]

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free. If you would like to support my writing, you can by upgrading to paid.

☀️ Here are 3 research findings, and some music, to consider this week (plus 🐶 pic)

2 IDEAS FROM RESEARCH

I.

A new AI tool provides another step towards speeding up drug discovery. 

AlphaProteo is an AI tool developed by DeepMind at Google that designs new proteins capable of binding to specific molecules in the body. 

“Like a key to a lock, one protein can bind to another, helping regulate critical cellular processes”. 

It’s easy to imagine how this technology could be used by researchers to develop treatments that precisely target problems in diseases like ME/CFS and Long COVID.

Imagine if it was used on the growing base of targets for post viral diseases- to help reduce inflammation, clear lingering viral particles, or improve energy production in cells!

While these applications are still theoretical for post viral illnesses, AlphaProteo brings the potential to speed up drug discovery and make real progress toward new treatments

Read more here about AlphaProteo

​II.

A very interesting finding from this CDC study by Elizabeth Unger, published in July:

Our findings suggest that COVID-19 is no more likely than other acute infections to be associated with ME/CFS.

As Healthrising nicely put it in Common Pathogens are as Bad as COVID-19 in Creating ME/CFS:

What a turnaround for the medical establishment this is. Many people with ME/CFS know how hard it’s been to convince doctors that a simple cold [or other common bug] could result in a disabling disease. It just didn’t compute.

This is another step towards legitimising postviral illnesses in the eyes of skeptical medics. 

III.

I find it great to see the real human faces of researchers on the front lines and to hear them talk about what they’re working on – and so I enjoyed this post from a leading German research group led by Prof. Carmen Scheibenbogen (English subtitles).

» Watch here « (scroll down to see the videos)

There are 2 short videos, discussing where they are in finding a diagnostic biomarker by measuring blood flows, blood cell deformity and microclots. 

E.g. How are cell morphology and cell deformability possibly related to microclots in ME/CFS? 

The second video is the latest update, although both videos are interesting- one with the celebrated lead researcher and the next with an up-and-coming researcher (the translation is admittedly a bit quirky, but that’s part of the fun!)

Thanks to all the amazing researchers working towards finding the answers, step by step 🙏 

1 THOUGHT

For Father’s Day recently I shared some peaceful piano music I’ve been making, with my old man… Here for your pleasure if that’s your cup of tea:

1 QUESTION FOR YOU

No questions for you this week - have a great week!

puppy p.s. Dreaming in the springtime (southern hemisphere!)

[alt: Whisky the cream toy poodle lies on a wooden deck, soaking up the sun]

Wishing you a peaceful week,

Tom and Whisky

☺️

This newsletter is and always will be free. If you would like to support my writing, you can by upgrading to paid.