r/CFSScience • • Mar 03 '24

"Scientist Shares Research Findings! Unveils Novel Mechanism for Chronic Illness: CFS/FM/POTS/MCS/LC" - YouTube

0 Upvotes

https://youtu.be/d3hh2l0bvac?si=99JbtKKIxTh4yu23

I used claude.ai to summarize the transcript of the above 2+ hour video:

TLDR:

  • The speaker became ill after chemical exposures and has researched the environmental causes of chronic illnesses like CFS, fibromyalgia, and MCS.

  • He argues these conditions are damage-based and caused by environmental factors like mold, VOCs, and nanoparticles damaging barriers and nerves.

  • Nanoparticles like titanium dioxide from consumer products are a major proposed cause. They circulate indefinitely and act as an internal "scrubbing mechanism" that mechanically tears tissues.

  • The speaker shares novel TEM imaging of skin showing apparent mechanical damage to myelin and barrier cells, supporting his theory nanoparticles induce the conditions by enabling damage.

  • He argues environmental science needs to be a large part of medicine to understand population effects and improve treatments. Simple patient surveys can quickly identify helpful therapies.

  • The speaker hypothesizes a 3-part therapeutic approach: repair barriers by minimizing VOCs, remove nanoparticles through blood draws, improve regeneration once damage is repaired.

  • Overall, he hopes spreading awareness of environmental damage will help patients immediately and drive more research into his proposed mechanisms.

Detailed summary:

The video discusses the speaker's research into the environmental causes of chronic illnesses like chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivity.

The speaker introduces himself as a scientist who got sick in 2017 after chemical exposure at work. He has since struggled with debilitating health issues and has done extensive research trying to understand the root causes.

He explains that there is little understanding of what causes these types of chronic illnesses, even though they affect millions of people. He aims to propose a novel mechanism for how they are induced, with a focus on environmental factors that researchers have ignored.

The speaker shares statistics showing a major rise in chronic illnesses over the past century. He argues this cannot be explained by genetics or viruses alone, and believes environmental factors are the missing link.

He explains his credentials and background as a scientist, and tells his story of how chemical exposure at work led to his chronic health decline. He describes his frustration with the medical system's dismissal of environmental factors.

The speaker emphasizes these illnesses represent a state of damage, not dysfunction. He argues even mitochondrial dysfunction is a downstream effect, not a root cause. The medical focus should be finding and addressing the upstream causes of the damage.

He proposes chronic viral infections like long COVID likely trigger the same downstream effects as other infections tied to chronic fatigue syndrome. He believes the distinction between diagnoses like CFS and long COVID is political, not medical.

The speaker outlines a model for how chemical exposures can damage epithelial barrier cells in the body, allowing toxins to enter and trigger chronic illnesses in genetically susceptible people. Damaged barriers also leave nerves vulnerable, like the vagus nerve.

He describes how repeated chemical exposures can worsen barrier damage over time, eventually leading to extreme sensitivity. He shares his own experience of becoming sensitive to everyday products like bandaids after repeated damage.

The speaker emphasizes these sensitivities represent real physiological damage, not psychosomatic effects. He advises against programs like DNRS that treat sensitivities as neurological. Avoidance of triggers is critical.

He summarizes the three main categories of toxic exposures that can contribute to chronic illnesses: mold, VOCs, and insoluble nanoparticles like titanium dioxide. He hints nanoparticles are a novel contributor he will expand on later.

The speaker shifts focus to discussing the induction of chronic fatigue syndrome and fibromyalgia in people who already have compromised epithelial barriers. He believes nanoparticles, especially titanium dioxide, are the primary factor driving these chronic illnesses.

He explains that exposure to insoluble nanoparticles like titanium dioxide results in connective tissue damage, impaired perfusion, and clogged lymphatics. Titanium dioxide is used extensively in consumer products like sunscreen, food, pills, paints, etc. It has a very long half-life in the body.

The speaker argues that nanoparticles act as an internal "scrubbing mechanism", slowly and physically digging into and tearing away at connective tissue, nerves, etc. This is supported by patient reports of feeling like there is "cement in my blood." The nanoparticles are literally circulating and causing damage.

He focuses specifically on titanium dioxide nanoparticles from matte white paint as a major source of exposure, since they continuously circulate in indoor air and are inhaled. He uses an analogy of gluing sand to paper to explain how the nanoparticles shed from the paint over time.

The speaker highlights a study showing titanium dioxide exposure creates chronic fatigue syndrome-like illness in mice. He argues the nanoparticles induce connective tissue damage that impairs perfusion, nerves, and more throughout the body. This explains the heterogeneity in symptoms between patients.

He shares personal experiences like needing sheet lifters at night to keep pressure off his arms, which get severely exacerbated by any mechanical force. This indicates to him a problem with connective tissue. He also shows photos of skin damage he attributes to titanium dioxide impairing cellular junctions.

Overall, the speaker argues that the variety of symptoms affected points to an indiscriminate, mechanical cause like nanoparticles, versus one particular molecular dysfunction. He believes chronic fatigue syndrome represents systemic silicosis without fibrosis. The nanoparticles directly cause the damage.

The speaker shares results from novel transmission electron microscopy (TEM) imaging he conducted on a skin biopsy sample. TEM allows viewing subcellular components at very high magnification.

He identified two abnormal cell types in the images. First, Schwann cells surrounding myelinated nerves contained large masses and black dots likely indicating glycogen deposits and dysfunction. Some masses were pressing on and distorting nerves.

Second, pockets were seen within the myelin layers. Experts agreed this indicates mechanical damage like tears in the myelin. The speaker argues this connects to his theory that titanium dioxide nanoparticles are mechanically damaging tissue.

He also saw abnormal glycogen deposits in keratinocytes, cells that form the epithelial barrier. This could explain the barrier dysfunction enabling nanoparticle uptake. Overall, the TEM imaging provides evidence supporting his proposed mechanism of barrier damage enabling particle intake that then causes neurological symptoms.

The speaker states the images may also show direct evidence of nanoparticles, though he cannot conclusively identify them. He argues the results warrant further research into nanoparticles playing a key role in chronic illnesses.

He closes by sharing survey results on beneficial treatments for ME/CFS, arguing simple surveys can more quickly improve patient quality of life versus long clinical trials. He also shares survey data showing 80% of ME/CFS and MCS patients have the other condition, indicating a strong overlap.

In conclusion, the speaker emphasizes environmental science should be a large focus of medical research to understand population-wide effects and find answers. He hypothesizes barrier repair, nanoparticle removal, and improving regeneration could treat these conditions. Overall, he hopes spreading awareness of his proposed mechanisms will help patients and spur future research.


r/CFSScience • • May 22 '24

“Clean Energy”: Can a Ketogenic Diet Help with ME/CFS and Fibromyalgia? - Health Rising (Apr 6, 2015)

2 Upvotes

https://www.healthrising.org/blog/2015/04/06/clean-energy-ketogenic-diet-chronic-fatigue-fibromyalgia-courtney-craig/

This blog is from 2015.

Summary by Claude.ai:

  • The author, a ME/CFS patient in remission, experienced a severe relapse in January after a series of illnesses and injuries.

  • Despite their usual treatments, the relapse persisted until they shifted to a high-fat, ketogenic diet, consuming 80% of calories from healthy fats.

  • Ketogenic diets, first used in the 1920s for epilepsy, are now being studied for various neurological disorders and cancer.

  • In a ketogenic state, cells burn ketones derived from fats instead of glucose from carbohydrates, producing less cellular stress and free radicals.

  • The author presents three reasons why ME/CFS and fibromyalgia patients should consider a ketogenic diet:

    1. Mitochondria: Ketogenic diets reduce free radical damage, improve mitochondrial function, and increase glutathione synthesis.

    2. Immune system: Fasting and ketosis can stimulate hematopoietic stem cells and may enhance the effects of drugs like Rituximab.

    3. Neuroinflammation: Ketones can downregulate inflammatory molecules (IFNγ, leptin, IL-6, IL-1β) and increase BDNF production in the brain.

  • The author, Dr. Courtney Craig D.C., was diagnosed with CFS in 1998 and recovered in 2010 using both conventional and integrative medicine.


r/CFSScience • • Aug 01 '25

Any paid research trials for ME/CFS?

5 Upvotes

r/CFSScience • • May 31 '24

I got a lot worse on methylphenidate

4 Upvotes

Has anyone experienced a decline in work performance when taking methylphenidate? When I take atomoxetine or drugs that increase noradrenaline, my ability to handle tasks improves significantly, while drugs that increase dopamine have the opposite effect. (I felt the same with Abilify, etc.)

I also have CFS and drug hypersensitivity (I think I have an underlying autoimmune disease), but what about my brain and body? Am I in the minority who experience a dramatic decline in concentration (getting caught up in fun activities and ending the day) when using methylphenidate? There were days when I used my smartphone for more than 22 hours straight. Dosage is minimal. (Also, I have a changed constitution, and all psychotropic drugs are immediate at the minimum dose. SSRIs and atomoxetine, which are said to cause nausea in 2-3 weeks, should also be taken at the minimum dose. Dramatic) It starts to have an effect after a few hours, but 18mg of methylphenidate is too much (prescribed as Concerta in Japan).

What I want to cure the most is CFS, and taking medication that boosts noradrenaline improves both my CFS and my ADHD, so I want to keep taking it, but I'm hypersensitive to the medication and it makes me feel like I have heart failure, so I can't continue.

With this kind of constitution, is there any way for me to improve my CFS and ADHD (if I had to choose, I would overwhelmingly cure CFS)? (Even something trivial would be fine. Even minor methods like antiviral drugs are welcome.)


r/CFSScience • • Nov 28 '25

An analysis of the possible geography of me/cfs, based on web search data.

7 Upvotes

r/CFSScience • • Aug 10 '26

How far are we from effective treatments?

12 Upvotes

Realistically, how many years away are we?


r/CFSScience • • May 11 '24

Hyperbaric oxygen therapy improves neurocognitive functions and symptoms of post-COVID condition: randomized controlled trial, 12 July 2022

6 Upvotes

Study

S4ME thread where they're pretty critical of the study.

Health Rising article on the potential of HBOT as a Long COVID and ME treatment.

Summary by Claude.ai:

  • This was a prospective, randomized, double-blind, sham-controlled clinical trial evaluating the effects of hyperbaric oxygen therapy (HBOT) on patients suffering from post-COVID-19 condition (persistent symptoms at least 3 months after infection)

  • 73 patients were randomized to receive either 40 daily sessions of HBOT (100% oxygen at 2 ATA for 90 minutes) or sham control (21% oxygen at 1.03 ATA)

  • Primary outcome: HBOT led to significant improvement in global cognitive function (medium effect size), specifically in attention and executive function domains, compared to controls

  • Secondary outcomes:

    • HBOT improved energy levels, sleep quality, psychiatric symptoms (depression, anxiety, somatization), and pain interference (large effect sizes) compared to controls

    • Brain imaging showed HBOT increased cerebral blood flow and induced microstructural changes in gray and white matter regions associated with cognitive and emotional processing

    • Clinical improvements correlated with brain perfusion and microstructural changes

  • The beneficial effects of HBOT may be attributed to its ability to induce neuroplasticity, increase brain perfusion, and modulate pathways involved in neuroinflammation, mitochondrial dysfunction, and tissue repair

  • HBOT was safe and well-tolerated with no significant difference in side effects between groups

  • Study limitations include relatively small sample size and lack of long-term follow-up data

In summary, this randomized controlled trial provides evidence that HBOT can improve neurocognitive functions, fatigue, sleep, psychiatric and pain symptoms in patients suffering from post-COVID-19 condition, potentially via induction of neuroplasticity and cerebral perfusion changes.


r/CFSScience • • Feb 05 '25

CFS caused by hemolytic anemia (Pyruvat kinase defiency) through lack of ATP / Mitochondrial Dysfunction

21 Upvotes

Hemolytic anemia causes the same symptoms like CFS through a lack of ATP. That is already well known in Pyruvat kinase defiency.

Look back at 1968: https://pubmed.ncbi.nlm.nih.gov/5658388/

Red blood cells have Atp as only energy source for their ion pumps and are 100% dependent from Mitochondrial expression. Klaus Wirth is leading in treatment for CFS in germany, check out mitodicure. https://mitodicure.com/science/

Also helpful https://drmyhill.co.uk/wiki/CFS_-_The_Central_Cause:_Mitochondrial_Failure#Chronic_fatigue_syndrome_is_the_symptom_caused_by_mitochondrial_failure

As well as https://en.wikipedia.org/wiki/Pyruvate_kinase_deficiency

Symptoms are very good in Picture in https://en.m.wikipedia.org/wiki/Anemia#/media/File%3ASymptoms_of_anemia.png


r/CFSScience • • Mar 04 '24

S4ME News in Brief - Week beginning 26th February 2024

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2 Upvotes

r/CFSScience • • Jul 28 '25

Danish Researchers Develop Novel 5-Minute ECG Method to Detect ME/CFS

18 Upvotes

r/CFSScience • • May 25 '24

Could the immune stimulating supplement OXYMATRINE be an effective treatment for long COVID?

10 Upvotes

ME/CFS expert Dr John Chia uses the antiviral immune stimulating herbal extract oxymatrine to treat his ME/CFS patients with enterovirus infections. Some of his enterovirus patients make major improvements on oxymatrine within a month or two of starting treatment. Oxymatrine seems to have an antiviral immune action against enterovirus. Dr Chia's oxymatrine ME/CFS study is detailed in this post.

Could oxymatrine also have antiviral effects against the SARS-CoV-2 coronavirus?

Coronavirus and enterovirus both fall into the same category of positive-sense single-stranded RNA viruses (+ssRNA).

Lots of +ssRNA viruses are linked to chronic fatiguing illnesses, including enterovirus, SARS-CoV-2, SARS-CoV-1, hepatitis C virus, dengue virus, Ross River virus and West Nile virus. So it's perhaps not entirely surprising that SARS-CoV-2 can also cause a chronic fatiguing illness.

Oxymatrine is known to work for the the fatiguing illnesses of enterovirus ME/CFS and known to work chronic hepatitis C virus infection.

So conceivably if oxymatrine works for enterovirus ME/CFS and hepatitis C virus, it might also have benefits for long COVID ME/CFS.

Oxymatrine can be bought as a supplement without prescription in the form of Equilibrant (Dr Chia's own formulation), and as the White Tiger brand of oxymatrine.

Dr Chia says oxymatrine treatment begins by taking half an Equilibrant capsule for the first week or two, then slowly increasing up to 2 or 3 capsules twice daily (a total of 4 to 6 capsules daily). See this video interview with Dr Chia at 4:24. Dr Chia says no escalation of dose should be made if there is a significant increase in symptoms (wait until the symptoms settle to increase the dose).

Though Dr Chia advises that oxymatrine should not be used for people with autoimmune tendencies (for example, a strong family history of autoimmune diseases, and/or if the patients have joint pain with positive rheumatoid factor and persistently positive ANA).

Further info on oxymatrine:


r/CFSScience • • May 26 '24

Oxaloacetate: the Best Mitochondrial Supplement for ME/CFS (and Long COVID?) - Health Rising (Oct 6, 2021)

11 Upvotes

https://www.healthrising.org/blog/2021/10/06/oxaloacetate-mitochondrial-supplement-chronic-fatigue-long-covid/

TLDR by Claude.ai:

In a preliminary study, Dr. David Kaufman found that oxaloacetate (OAA) supplementation significantly reduced fatigue in ME/CFS patients, with 80% reporting improvement. While promising, the high cost of OAA and the lack of placebo-controlled trials means more research is needed to confirm its effectiveness in treating ME/CFS and related conditions.

Longer summary by Claude.ai:

  • Oxaloacetate (OAA) is a supplement that may help with mitochondrial problems in ME/CFS and fibromyalgia.

  • Dr. David Kaufman became interested in OAA after a 2017 metabolomics study found it was significantly depleted in ME/CFS patients.

  • Kaufman conducted his own in-house study with 52 ME/CFS patients, giving them either 500mg or 1,000mg of OAA twice daily.

  • Results showed significant reductions in fatigue scores, especially on the Chalder Fatigue Scale, with higher doses appearing more effective.

  • Kaufman called the results "striking and surprising," with 80% of patients reporting improvement and few side effects.

  • The main drawback is the high cost of OAA supplements, around $500-600 per month at effective doses.

  • Placebo-controlled trials are needed to confirm the benefits of OAA in ME/CFS.

  • OAA studies are also underway for Alzheimer's, ALS, myasthenia gravis, cancer, and long COVID.


r/CFSScience • • Jul 30 '25

Intermittent fasting and a no-sugar diet for Long COVID symptoms: a randomized crossover trial

12 Upvotes

r/CFSScience • • Dec 25 '25

Are we close to figuring it out?

14 Upvotes

So, are we close to finding why this disease happens? How is it possible that is 2026 and we stil have no idea of what causes this hellish illness?


r/CFSScience • • Jun 16 '24

S4ME News in Brief - Week beginning 10th June 2024

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4 Upvotes

r/CFSScience • • Aug 10 '26

SARS-CoV-2 ORF7a drives mitochondrial dysfunction via PDK4 activation and complex I inhibition

27 Upvotes

This study was summarised using Gemini AI.

The study investigates how the SARS-CoV-2 accessory protein ORF7a manipulates host cell metabolism to create an environment that favors viral replication and immune evasion. Normally, healthy cells rely heavily on mitochondria to efficiently produce energy through a process called oxidative phosphorylation. However, the researchers discovered that the ORF7a protein essentially short-circuits this system, forcing the cell to rely on a less efficient, glucose-heavy energy pathway called glycolysis.

Cellular Changes Induced by ORF7a

FeatureHealthy Cell BaselineORF7a-Infected Cell
Primary Energy SourceMitochondrial respirationGlycolysis (Warburg-like effect)
Oxidative Stress (ROS)Balanced by antioxidant defensesHighly elevated due to depleted glutathione
PDK4 Enzyme LevelsNormal baselineSignificantly up-regulated
Mitochondrial Complex IFully active and assembled into supercomplexesFunctionally impaired and structurally disassembled

Key Mechanisms of Mitochondrial Sabotage

The researchers identified two primary ways that ORF7a breaks the cell's mitochondrial engine:

  • The PDK4 Roadblock: ORF7a causes a massive increase in the enzyme PDK4. PDK4 then phosphorylates and turns off the Pyruvate Dehydrogenase Complex (PDHC). This effectively acts as a roadblock, stopping pyruvate (the cell's standard fuel) from entering the mitochondria to be burned for energy.

  • Direct Complex I Impairment: Independent of the PDK4 roadblock, ORF7a selectively cripples "Complex I," a crucial piece of the mitochondrial electron transport chain. It also stops these respiratory complexes from assembling together properly.

  • Irreversible Damage: When scientists treated the cells with a drug called dichloroacetate (DCA) to remove the PDK4 roadblock, mitochondrial energy production still failed to recover. This proved that the damage to Complex I is a separate, profound disruption caused by the virus.

  • Oxidative Stress: Because the mitochondria are malfunctioning, they leak reactive oxygen species (ROS), and the cell's natural antioxidant buffers (like glutathione) are depleted, leading to severe cellular stress.

Key Takeaway

The SARS-CoV-2 ORF7a protein cripples the host cell's mitochondria via a "two-pronged attack"—blocking fuel entry by activating PDK4 and destroying the engine itself by impairing Complex I. This forces the cell into an inflexible, stressed, glucose-burning state that likely fuels the severe inflammation and metabolic complications seen in COVID-19 patients.

Link to 2026 study


r/CFSScience • • May 22 '24

Mitochondrial Enhancers for Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Pt. I: D-Ribose, CoQ10 and PQQ - Health Rising (Dec 18, 2020)

15 Upvotes

https://www.healthrising.org/blog/2020/12/18/5mitochondria-coq10-d-ribose-fibromyalgia-chronic-fatigue-syndrome/

TLDR by Claude.ai:

The article discusses the potential role of mitochondrial dysfunction in chronic fatigue syndrome (ME/CFS) and fibromyalgia (FM). While some studies have found issues with the mitochondria, the results have been inconsistent. The article explores various mitochondrial enhancers such as D-Ribose, PQQ, CoQ10, and NADPH, discussing their potential benefits and usage. However, it concludes that effective treatment of ME/CFS and FM likely requires a comprehensive approach addressing nutrition, metabolism, triggers, stressors, and physical activity as an integrated system.

The gist, copied from the blog:

  • Studies suggest problems with energy production exist, but we still don’t know why.

  • The mitochondria – the main energy producers of the cell – are a possibility. A variety of mitochondrial problems have been found, but the study results have been inconsistent.

  • Since we don’t know which parts, if any, of the mitochondria have problems in ME/CFS/FM, it’s impossible to precisely target the mitochondria.

  • Plus, if problems outside of the mitochondria exist – such as reduced oxygen delivery to the tissues or hydrogen sulfide issues – then enhancing mitochondrial production may not help.

  • Still, quite a few ME/CFS doctors do recommend mitochondrial enhancers, and some study results suggest they may be helpful.

  • D-Ribose – By bringing purines and pyridimines together, D-Ribose provides the underpinnings for important substances such as DNA, RNA and ATP.

  • D-Ribose levels decline during the low oxygen states which may be present in ME/CFS and FM. When those conditions are present, cells turn to bringing two ADP molecules together to form ATP. The AMP left over is washed out – leaving the cell depleted in purines. Bob Naviaux found reduced purines in ME/CFS.

  • D-Ribose is able to enhance purine levels. Two non-placebo blinded studies from Dr. Teitelbaum suggest the D-Ribose may be helpful in a number of ways.

  • Several ME/CFS doctors recommend using 3 scoops of D-Ribose a day for several weeks and then dropping down.

  • PQQ – is a mitochondrial generator, nerve cell protector, an anti-inflammatory, and is able to protect the mitochondria from oxidative stress.

  • PQQ may be able to improve short-term memory, attention and information processing.

  • PQQ may work better when taken with CoQ10. Doses appear to be around 10-20 mgs/day

  • CoQ10 – arguably the most important mitochondrial enhancer, CoQ10 carries electrons from one part of the electron transport chain to the other, and it reduces oxidative stress. It’s used in a number of diseases.

  • Several studies have found low CoQ10 levels in ME/CFS and FM, and several trials suggest it could help.

  • CoQ10 comes in two forms: ubiquinone and ubiquinol. Ubiquinol is best absorbed and is recommended particularly as we age. It’s more expensive, but less is needed.

  • It may take up to a month for CoQ10 levels to plateau while taking ubiquinol 2-300 mg/day. It should be taken with fats. Be wary of taking it before bedtime.

  • NADPH – does not appear to be used as a mitochondrial enhancer, but it’s mentioned here because Bob Naviaux focused on it with regards to the metabolism in ME/CFS.

  • He believes that all the metabolic abnormalities found in ME/CFS may be a consequence of redox issues or reduced levels of NADPH.

  • Naviaux calls NADPH the cellular barometer of metabolic stress, but does not recommend NADPH supplementation.

  • Instead, he reports that theoretically, incremental improvements in NADPH could be produced with folate, B12, glycine, serine pools, and B6 metabolism.

  • Mitochondrial enhancers probably work best when used together and in conjunction with a program to treat ME/CFS/FM.


r/CFSScience • • Aug 23 '26

Where is the experience of fatigue located in the brain?

5 Upvotes

I am so exhausted and too fatigued to write a proper post right now, but I personally believe that the very fatigue most of us are experiencing stems from the brain region responsible for diminishing/shutting down activity of the organism when certain conditions are met, especially chronically activated or even when those certain conditions are no longer exist.

There is also a theory from Ronald W. Davis, from Human Genome Project whose own son named Whitney Dafoe dealing with ME/CFS since 2007 afaik, named as "Itaconate Shunt Hypothesis".

I am creating this post to probe the ideas and discussions by people familiar with these, or willing to explore and digest the publications and discuss about the origins of the fatigue we are experiencing.

As I have said, I am so fatigued and my brain fog is so intense that I was only be able to compose such a scattered post, sorry for that.

Image is taken from the publication:

Brain and muscle chemistry in myalgic encephalitis/chronic fatigue syndrome (ME/CFS) and long COVID: a 7T magnetic resonance spectroscopy study https://www.nature.com/articles/s41380-025-03108-8


r/CFSScience • • May 16 '24

Close relationship between CFS and fibromyalgia, and TCA

5 Upvotes

Hello

I'm Japanese and I'm writing this using Google Translate (I'm sorry if my English is clumsy)

I believe that CFS and fibromyalgia are closely related.

I'm having a lot of trouble with cfs, and I can't move all day because of brain fog, and my days are like hell.

Meanwhile, TCA (especially Nortriptyline) was effective and my body felt really good. (Also, maprotiline was also very effective, so I felt that increasing noradrenalin was necessary for me.)

However, I am very sensitive to drug side effects, and just 10mg of Nortriptyline caused significant QT prolongation, and I had exactly the same result with maprotiline.)

I have a particularly sensitive reaction to cyp2d6 drugs.

In this case, what medicine do you think is effective for CFS and fibromyalgia and that even I, who is not sensitive to medicine, can take?

(I also took mirogabalin and pregabalin, but my vision deteriorated so much that I couldn't take them. I'm really sad.)

What I'm going to try now is a low dose of Duloxetine and a low dose of Desvenlafaxine. (I feel like this probably won't work either...)

I also have the ridiculous idea of ​​implanting a defibrillator and using TCAs, since they work best (but risk QT prolongation and heart attack).Is this really an extreme idea?


r/CFSScience • • May 25 '24

Mitochondrial Enhancers for ME/CFS and Fibromyalgia Pt IV: N-Acetyl Cysteine (NAC) - Health Rising (Sep 9, 2021)

18 Upvotes

https://www.healthrising.org/blog/2021/09/09/mitochondrial-enhancers-chronic-fatigue-fibromyalgia-nac-n-acetyl-cysteine/

TLDR by Claude.ai:

N-acetyl cysteine (NAC) is a powerful antioxidant that can boost levels of glutathione, the body's master antioxidant. NAC appears to work primarily in the mitochondria, reducing oxidative stress and potentially enhancing ATP production. Dr. Dikomo Shungu's research has shown that ME/CFS patients have low brain glutathione and high lactate levels. In a pilot study, NAC supplementation normalized these levels and improved symptoms. Shungu is currently conducting a larger, NIH-funded clinical trial to further investigate the effects of NAC in ME/CFS. While NAC shows promise, more potent antioxidants and improved delivery methods are under development, offering hope for future treatments.

The gist, copied from the blog:

  • N-acetyl cysteine or NAC has been called the “epitome of antioxidants”.  Able to rejuvenate the levels of the most powerful antioxidant in the body – glutathione – appears to do its work mostly in the mitochondria.

  • That’s good news as the mitochondria are the greatest free-radical producers in the body and dysfunctional mitochondrial – such as may be found in ME/CFS – can produce enormous amounts of oxidative and nitrosative species (otherwise known as freed radicals).

  • How exactly NAC works has not exactly been clear but recent research indicates that NAC also triggers the production of hydrogen sulfide which, in turn, produces antioxidant effects and perhaps enhances ATP production as well.

  • Dikomo Shungu of Cornell University parleyed small pilot grants from the Solve ME Initiative into millions of dollars of NIH funding, and ultimately, a rare NIH-funded clinical trial, Shungu showed that ME/CFS patients’ brains contain low glutathione and high lactate and oxidative stress levels.

  • Shungu’s preliminary study found 1800 mg NAC supplementation returned glutathione, lactate, and oxidative stress levels to normal and helped with symptoms in ME/CFS.

  • In 2020 Shungu received a large NIH grant to study the effects of 900 mg and 3600 mg of NAC daily for four weeks on symptoms, glutathione, lactate, and oxidative stress levels in ME/CFS. Particularly at the higher dose level, Shungu is using far higher doses than we ordinarily see in ME/CFS. Shungu’s study is expected to run through 2025 and is still open. (See blog for details).

  • Shungu does not believe the mitochondria are damaged in ME/CFS. His studies suggest to him that ME/CFS is an oxidative stress-induced micro-circulatory disease. Oxidative stressors are shutting down the blood vessels – preventing proper amounts of oxygen from getting to the mitochondria.

  • More effective ways to deliver NAC are under development which may be far more potent. New forms of antioxidants such as cysteamine are popping up as well which may be able to better boost antioxidant levels in the body.  Hydrogen sulfide is a particular area of interest that Health Rising will delve into. Plus, a new and perhaps dramatically more potent form of the master antioxidant in the body is coming to market. Health Rising will have a blog on that as well.


r/CFSScience • • Feb 01 '26

USA Bloodwork Guide I have been working on

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6 Upvotes

r/CFSScience • • Jul 08 '24

Mitodicure - new article

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6 Upvotes

r/CFSScience • • Feb 12 '24

New study shows heightened mitochondrial respiration correlates with LC severity and likelihood

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7 Upvotes

r/CFSScience • • Sep 05 '26

Beyond genes: EpiSwitch® and Orion platform-powered 3D genome architecture biomarkers reveal shared biology across ME/CFS, long COVID, PTSD, rheumatoid arthritis, and multiple sclerosis - Journal of Translational Medicine

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24 Upvotes

"Analysis of the ME/CFS dataset identified 552 unique 3D genomic anchors mapped to 567 genes, with analogous disease-specific anchor sets generated for LC19, PTSD, RA, and MS. Direct overlap between disease-associated genes was limited; however, higher-order network analyses revealed substantial interconnectivity and convergence across conditions. Shared biological pathways included immune and cytokine signalling, interferon responses, mitochondrial function, metabolic regulation, and neuroendocrine processes. Highly connected hub genes included immune regulatory nodes such as LAG3 and components of the mTOR signalling pathway, implicating T-cell exhaustion, chronic immune activation, and immunometabolic dysregulation as common mechanisms underlying these disorders."