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@remissionbiome

@PeterAttiaMD

@remissionbiome

@remissionbiome

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🕸️Dr.T, PhD

@chydorina

Jan 9

Yesterday's article showing how Ambien/a z-drug ( benzodiazepine type sedative) negatively affects glymphatic clearance needs to be addressed and the potential consequences need to be carefully deconstructed especially in light of how common their use is in MECFS LongCovid and other chronic illnesses.

Its not fearmongering. I do think there is a major issue here and improper use might be one of the most dangerous things we can do in terms of our long-term cognitive health.

Its not just glymphatic clearance that is being negatively affected.

Benzo-type sedatives also affect brain wave patterns. Studies from way back in the 60s showed that they increased beta waves. Its a paradoxical effect - we feel like we are less anxious when we are on them but our brains are actually in fight-flight.

This recent paper on the negative effects of Ambien (which will likely apply to more benzodiazepine type drugs) on glymphatic clearance is a major issue especially in MECFS.

Pretty much the only intervention we know of that can help reduce the severity of PEM crashes from developing when used in moderation and very infrequently has potentially disastrous consequences if used improperly long-term. And this is not even taking into consideration the potential for serious adverse consequences of withdrawal and how difficult it is for people who have been on them for prolonged period to stop.

I was put on benzos (both Clonazepam and Lorazepam) for over a decade, with full physician oversight and was told that I would likely always need to be on them (I started prior to my second bout of MECFS). The reason was constant sympathetic nervous system overactivation (c-PTSD). Tapering and getting off of them took years in my case. I am now at a place where I can use lorazepam infrequently and do so for major crash inducing activities - but I try very hard to keep my use lower than a few times a month.

I would think this issue would be getting WAY more attention than it does - I guess we are all just too afraid to discuss it (let alone think about it) given that it is considered the only option my many people for PEM crashes and sleep.

The risk:benefit however is very seriously on the side of risk - especially when used daily for long periods of time. The bottom line here is that we just dont know how risky this medication might be in terms of long-term cognitive decline - but the literature is stacking up that the risk might be very considerable.

Sleep dysfunction and glymphatic clearance are among the biggest potential issues in MECFS that make recovery difficult. Without proper sleep we cannot heal. Many of us use these medications for sleep as MCAS and histamine and mast cell dysfunction directly affects our circadian rhythms and increases insomnia and its the only thing that helps. I know many of us would be seriously hooped if we didnt have access to benzodiazapines.

Finding alternatives is of paramount importance and should be one of the very top clinical priorities in MECFS and LongCovid research.

We should not be forced into taking a drug that can lead to cognitive decline and dementia (the potential ultimate consequence of dysfunctional glymphatic clearance as is suggested by much of the literature) to help us sleep and help control the severity of PEM.

That this is literally the only option that is available and it is potentially this damaging when used long-term and continuously is frankly completely unacceptable.

Like using chemo to treat cancer, how much unnecessary damage are we doing to ourselves - under the guise of 'treatment'.

I know this issue will be very scary for people to think about and i apologize as I know this will be triggering for a lot of people because there really are no good options.

But, it is too important to sweep it under the rug and we do need to discuss it.

How can we use benzo-type drugs are safely as possible given the potential consequences for glymphatic clearance and long-term cognitive decline should be a big conversation. Is there any safety margin or dose or is their use keeping us stuck in chronic illness and decline.

x.com/chydorina/stat…

https://x.com/chydorina/status/1436064278499381281

https://x.com/chydorina/status/1436064278499381281

https://x.com/EricTopol/status/1877395859228266511

https://x.com/EricTopol/status/1877395859228266511

Read 7 tweets

🕸️Dr.T, PhD

@chydorina

Dec 6, 2024

Toxoplasmosis infection is one of my opportunistic co-infections and the threat of it getting into the central nervous system (brain) is ever present (it can be a high risk in those that have immunosuppression as well as during pregnancy).

Its not a parasite that can really be successfully treated w/ current pharma drugs - they are not effective on all stages and can be much too hard on altered sick bodies dangerous as the mess with folate metabolism.

I use a Herbal protocol designed by master herbalist Dr. Stephen Buhner (search Buhner toxoplasmosis and you will find it) and I do a 21 day course 2-3 times a year. With addition of a few other herbs its also a good EVB herbal protocol.

I am always looking for alternate ways of keeping the toxo latent and making sure cysts dont grow. Probiotic mixtures that increase SCFAs - seem a useful add-on for anyone dealing with toxoplasmosis.

Probiotic-induced changes in intestinal microbiome inhibits Toxoplasma gondii infection
parahostdis.org/journal/view.p…

Multi-strain mixture composed of:

stephenharrodbuhner.com/wp-content/upl…

Read 4 tweets

🕸️Dr.T, PhD

@chydorina

Dec 1, 2024

We need an X prize for a biomarker(s) for #LongCovid.

Currently there are no well accepted clinical endpoints that can be used in clinical trials and this more than anything else is hampering research progress and drug development.

There has got to be a couple billionaires out there who would fund an X prize (or we just tap $1 from every person who has #LongCovid and run a few hundred X prizes). With 200+ million people globally, the demand/resource is there. Plus, it would be a billion dollar company eventually.

Special bonus prize of course for the marker also applying to #MECFS.

Home test/commercial test would be the goal.

All we really have right now are 'survey's' - questionnaires were people are asked questions like 'what is your level of fatigue'. This is not acceptable.

Research-only markers are not going to cut-it. Home testing is the goal (and if along the way we find a few that require more expensive tech, well it wont be a waste of time).

Read 9 tweets

🕸️Dr.T, PhD

@chydorina

Nov 29, 2024

"The patients taking the synbiotic reported a significantly superior drop in post-exercise malaise (68.0% on average) at 3-month follow-up as compared to the placebo group (37.5%)."

Small trial finds significant effect of probiotic mixture on PEM with increase of choline in the thalamus, creatine in white/grey front matter, and N-acetyl aspartate before/after

Synbiotic (probiotics+) trial worth mentioning. The trial may have been small (n=32) but the significance of the intervention on PEM was quite high. Interestingly there was no effect on 'fatigue' per se - it was actually Post-exertional malaise where the benefit was found.

What did they do? 3 months of a combo probiotic supplement that included:
- Lacticaseibacillus rhamnosus DSM 32550, -
- Humiome® Lactiplantibacillus plantarum DSM 34532 (formerly known as L. plantarum TIFN101),
- Bifidobacterium lactis DSM 32269,
- Bifidobacterium longum DSM 32946,
- FOS fructooligosaccharides (2.5 mg) - a 'pre-biotic'
- Zinc (5 g).

The effects of 3-month supplementation with synbiotic on patient-reported outcomes, exercise tolerance, and brain and muscle metabolism in adult patients with post-COVID-19 chronic fatigue syndrome (STOP-FATIGUE)

link.springer.com/article/10.100…

Read 5 tweets

🕸️Dr.T, PhD

@chydorina

Nov 18, 2024

You are competing RIGHT NOW for ENERGY with all the parasites and pathogens that are living on and in you. Yes, there are pathogens that can hijack the products of our mitochondria and co-opt ATP production for replication. In the process they will create more inflammatory reactive oxygen species, more systemic inflammation, and more dysfunction.

ENERGY production is a resource, and not one we have enough of a surplus of to share with pathogens - treat whole body pathogen load!

Treat what can be treated.

you eat, candida eats

Read 11 tweets

🕸️Dr.T, PhD

@chydorina

Oct 3, 2024

It is possible to have normal oxygen saturation and pathological hypoxia at the same time? In certain conditions like #ME and #LongCovid this is likely what is actually occurring. Some tissues (like brain and muscles) are not getting enough oxygen.

To make matters worse it is possible that epigenetic 'memory' of the sick state is part of what might keep us sick (even when an acute illness ends) - and that changes in oxygen gradients in tissues (pathological hypoxia) is a trigger for these epigenetic changes.

We don't have a definitive answer yet but interactions between inflammation + the immune system + pathological hypoxia (low oxygen) may provide some clues that this is indeed occurring.

It can be hard to wrap ones head around having low oxygen or hypoxia when your smart watch shows normal oxygen saturation.

BUT! It is oxygen USE that is the issue, not that it is there is the first place. When we look at oxygen getting to the brain and oxygen use in the muscles, we see a different story.

It is obvious that hypoxia would interact with the immune response and inflammation and changes oxygen gradients in different tissues.

"These changing oxygen gradients are exaggerated during inflammation, where oxygenation is often depleted owing to alterations in tissue perfusion and increased cellular activity."

Pathological hypoxia also interacts with Mast Cells - causing them to degranulate and release inflammatory meditators. Obviously those that have MCAS might need to pay particular attention to hypoxia as a risk factor to help manage Mast Cells.

If activity also restricts oxygen in brain and muscles this could be one reason why physical activity can lead not just to crashes but also MCAS flares and its maintenance when all other triggers have been removed. (note: mast cells can also release interferon-gamma!!).

Hypoxia potentially interacts with ME and LC disease processes in many ways, affecting inflammation, immune responses including mast cells, and even epigenetics. Hypoxia might induce epigenetic changes in immune cells, such as chromatin remodeling, which can have long-lasting effects leading to 'immune memory' and a change of state from pre-illness that is hard to turn back.

Practically, this means that immune cells exposed to hypoxia may retain a "memory" of this exposure, affecting their response to future infections or inflammatory signals.

"How oxygenation shapes immune responses: emerging roles for physioxia and pathological hypoxia"

link in comments: nature.com/articles/s4157…

potential interventions: compression pants and compression + external counterpulsation (EECP)
verywellhealth.com/enhanced-exter…

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