📢 “irisin protects against neuroinflammation by acting directly on glial cells in the brain”

Irisin is a peptide released by muscles after exercise.

It’s been identified as one of the reasons exercise helps cognition & works directly on microglia

hsci.harvard.edu/news/hormone-i… Given it’s released after exercise, people with #MyalgicEncephalomyelitis and #LongCovid with PEM may surely be considered to be low in circulating Irisin.

Importantly: “soluble irisin…is sufficient to confer the benefits of exercise on cognitive function”

There’s a *very* pragmatic and important reason why ME/CFS must be included in this.

At least 50% of pwLC meet the diagnostic criteria for ME. We know that.

With the end of funded covid testing, Long Covid as a diagnosis will dwindle. Ppl are already not getting LC diagnosed.

https://twitter.com/lcmoonshot/status/1777757870941233431

Moving forwards, more of those with covid induced-ME/CFS will either have no diagnosis or will be diagnosed with ME/CFS just as anyone else who develops it from an unknown cause.

Mixed in with them will be those with non-covid-ME/CFS from EBV etc that’s still happening.

This looks MUCH better than the usual very limited scales.

I’m glad the Moderate group isn’t quite so wide and I like the expansion of the Very Severe into sub categories.

https://twitter.com/tomkindlon/status/1777351143300993354

Oh and no wonder it’s good, co authors include Janet Dafoe, Whitney Dafoe and Ron Davis 😊

This is a marked improvement on previous severity groupings for #MEcfs

Check your choline intake: are you getting enough? #MEcfs #LongCovid

In people who have a variation of the PEMT -744 gene with one change from G-->C (rs12325817) 78% developed organ dysfunction when fed a low choline diet

pubmed.ncbi.nlm.nih.gov/16816108/ Choline deficiency is more likely in those with folate or B12 deficiency since choline is utilised more for methylation in the absence of those B vits.

Lack of choline leads the body to cannibalise it’s own cell membranes to keep blood levels above 50% ods.od.nih.gov/factsheets/Cho…

Revisiting this in depth metabolomics paper on ME/CFS.

Of the 6 such studies “common threads in the results from all these studies are decreased levels of phospholipids and metabolic dysregulation”
ncbi.nlm.nih.gov/pmc/articles/P… “we observed decreased levels of phospholipids, especially plasmalogens and phospholipid ethers”

My takeaway: Phospholipids may be crucial for pwME to supplement, even if they don’t touch symptom levels, but for basic cellular support.

@cstroeckw I think it could. I’ve just started a trial on myself. But there are good reasons why some pwME could react v badly also. It carries a risk of metabolic acidosis via pushing mitochondria into anearobic activity. Many of our mitochondria already do this too much anyway. @cstroeckw The main risks for a bad outcome on Metformin are 1) hypoxia and 2) poor renal clearance of lactate. We know from #TheAcidTest some pwME have poor lactate clearance as standard, and may have chronic hypoxia from poor blood flow.

Every now and then I find something about research on #MyalgicEncephalomyelitis that I didn’t know.

This one is particularly astonishing in terms of remmision events such as @remissionbiome are creating.



Has relevance for #LongCovid toome-pedia.org/wiki/Interfero… This research also shows that most of those with ME who ‘recover’ are in fact not recovered but remain at high risk of relapse. Which may prove the same for Long Covid.

So, highlights pasted in below:

I don’t think I mention this often enough as I see people describe this quite often:

If you get night sweats and adrenaline dumps at night, it’s very possibly caused by hypoglycaemia (low blood sugar).

When suga drops, adrenaline is released to compensate.

#MEcfs #LongCovid Blood sugar regulation is commonly messed up in #MEcfs #LongCovid #Fibromyalgia and #POTS

🚨**You can have sugar problems in these conditions even if your GP has done a HbA1c test and says you’re fine**

You need to use a continuous glucose monitor for a week or two to check.

Very interesting study here on the metabolic and muscle consequences of extreme bed rest.

For 60 days the participants weren’t even allow to sit up, or use a pillow to prop up, did they develop ME/CFS?

Of course they didn’t!!

https://twitter.com/therasmussenlab/status/1747346968030925245

““a 60-day strict 6° head-down bed rest. No pillows were allowed except for a thin cushion when participants lay on their side; one shoulder always had to touch the mattress, and all daily activities including personal hygiene were done in the −6° position”

This disease is like when someone is help captive & deprived of so much that when their captor eventually gives them just a grain of kindness & gives them back the smallest of privileges, like being able to clean themselves, or use a toilet, the captive is so grateful for it… that they become subservient & accept their situation.

It takes so much, repeatedly, that we lower and lower what standards we’d accept as ‘good’ & be grateful for them as though if we aren’t grateful, those small privileges will be taken away again #MyalgicEncephalomyelitis

Stumbled on this paper, which seems particularly relevant to #LongCovid form of #MEcfs given the findings from the NIH study showing the role of ER stress induced mitochondrial dysfunction in the disease.

Few quotes below ⬇️
sciencedirect.com/science/articl… “During evolution, SARS-CoV-2 have evolved strategies to escape immune responses by targeting ER and mitochondria.”

“COVID-19-related ER-mitochondrial stress is a major player in the promoting of cytokine storms and ARDS.”

Yesterday, I finally watched this video where a doctor in the States talks about how he approached treating a patient with POTS and reduced brain blood flow. It was quite emotional & interesting.

🧵 on what I took away Why emotional? Because here is someone who actually did what doctors should do; he tested & thought about it & tried to understand the pathology. He used evidence of blood flow & neurological tests at every step & fully understood the constraints lack of blood flow caused.

So, I’m pretty sure I have an iron deficiency that all my doctors have missed. And it’s likely many pwME and LC do too, because it’s hugely overlooked even in symptomatic patients.

I’ve put together a thread 🧵 to help inform other with #MEcfs #LongCovid & #Fibromyalgia This paper here is what I will cite in this thread. There are other papers but they’re mostly all cited in this one and I need to save my energy so I will just take from this one onlinelibrary.wiley.com/doi/full/10.10…

A warning to anyone thinking of trying the low PRAL diet: if you’re not in a state of acidosis, it could push you into alkalosis, which you also don’t want to be in.

So please be cautious, a diet may not sound too risky, but these diets do real things in the body #TheAcidTest

https://twitter.com/paulrkeeble/status/1664306002542444548

Personally the low PRAL diet won’t be something I will try.

My lactic acid levels are elevated, yes, but that does not mean acidosis.

Typically between 2-4mmol/l are not indicative of lactic acidosis unless blood pH is also acidic patient.info/doctor/lactic-…

Hmmm 🤔 blood tests result pinged in, my phosphate is 0.83mmol/L and the Serum phosphate normal range is 0.83–1.63 mmol/l in healthy adults. Right on the edge of low/not low. “Phosphate is involved in many critically important biochemical processes including energy metabolism, nucleic acid metabolism, cell signaling, bone formation, and maintenance of acid–base balance”

PI% info @PanickedFoodie @tessfalor

I’m always hot after I eat my evening meal so decided to check my PI and yep, best I’ve ever seen it (usually under 1.5)! Supports eating causing improved blood flow. But…my SPO2 is the lowest I’ve ever seen it. Never seen it go below 98% Only other times I’ve managed to improve my PI% have been my using a hot water bottle on my abdomen (but it only went from 1.5% to 5.7%), or by laying down in bed & heating myself with a hair dryer, where my PI% went over 15% for the first time.

Hospital trip yesterday about POTS. The doctor was also researcher in blood pressure so he was actually great & was very interested in the data I gave him on my BP, glucose & lactate. Couldn’t offer any help I haven’t already tried but ordered a ton of bloods & a tilt test. Unfortunately my blood didn’t want to come out & I ended up at the hospital an extra 2 hours & extremely stressed. They finally got some out but as usual the phlebotomist was amazed at how my blood simply wouldn’t come out.

Exercise is contraindicated for people with ME/CFS. Full stop.

Those with mild disease may be able to do some gentle exercise, or even occasional long walks, but the body simply doesn’t respond the way it should. Exercise = stress for the body. Healthy bodies adapt, ours don’t. Cardio exercise especially always carries risk for those with ME/CFS. Even when it’s mild. The usual benefits that healthy people experience from adapting to exercise don’t occur. Cumulative physical stress from regular exercise with ME/CFS may lead to a decline in condition.

Most of us are now familiar with #POTS but there are different types: hypovolemic, neuropathic & hyperadrenergic.

The hyperadrenergic form may be genetically determined & involves blood pressure increase when standing & elevations in adrenaline healthrising.org/blog/2018/08/1… “Grubb’s 2011 study described hyperadrenergic POTS as having an increase in systolic blood pressure of ≥ 10 mm Hg during a tilt table test with rapid heart beat (tachycardia) or serum norepinephnrine levels that were greater than 600 pg/mL upon standing”

“Compared to uninfected controls, COVID-19 patients of all age groups had severe GSH deficiency, increased OxS and elevated oxidant damage which worsened with advancing age. These defects were also present in younger age groups, where they do not normally occur”

https://twitter.com/renesugar/status/1610112505778700289

This study looked at 60 people hospitalised with SARS-CoV-2 and found severe glutathione deficiency in them, across all age groups.

Treatment with Glycine plus NAC may help to increase Glutathione and reduce oxidative stress.

In 2003, cardiologist Arnold Peckerman published this paper on #MEcfs using a non-invasive measure of cardiac🫀 output.

It showed patients with severe ME/CFS had significantly lower stroke volume & cardiac output, hence reduced circulation pubmed.ncbi.nlm.nih.gov/12920435/ The level of cardiac impairment correlates with the severity of the disability. Dr Peckerman surmised that those with severe ME/CFS have a form of heart failure (source webmd.com/chronic-fatigu…)