Dr Ron Davis - Updates on ME/CFS research - September 2019 onwards

There is only one well-known anecdotal report of a person being rediagnosed with MS and responding to Copaxone as per social media reports. The OMF is latching onto every anecdote as usual. I understand the desperation (aren't we all desperate?). That does not give you the right to spread dangerous misinformation/nonsense.

Post-exertional malaise is not a recognised medical symptom outside of the context of ME/CFS so of course it's not going to be listed as a symptom of MS or any other disease. However, fatigue is a recognised symptom of MS. ME/CFS is considered a diagnosis of exclusion so if your "fatigue" is explained by MS, then you have MS.

 

Exactly. We'd be dropping like flies and we'd have MRI evidence of disease. No one would be questioning our disability. We wouldn't even be on this forum.

 

Post-exertional malaise is recognised as a symptom in some patients with Long Covid (PASC).

If the September 2023 ICD-10-CM proposals currently under consideration by NCHS/CDC and supported by Patient-Led Research Collaborative and a number of US ME/CFS organisations is approved, patients coded with:

U09.9 COVID-19 condition, unspecified
> Post-acute sequela of COVID-19

who are identified as having symptoms consistent with PEM will be able to be assigned the proposed new Symptoms chapter code: R68.85 Post-exertional malaise as long as they do not also meet criteria for a diagnosis of G93.32 ME/CFS.

In accordance with ICD conventions, patients diagnosed with G93.32 ME/CFS would not be assigned the proposed new code: R68.85 Post-exertional malaise because PEM is a hallmark symptom of ME/CFS and is implicit within the G93.32 diagnosis code.


Once the R68.85 Post-exertional malaise code is approved, there is the potential for other diseases and conditions beyond Long Covid to also attract the PEM code (as long as the patients do not meet criteria for a dx of ME/CFS).


Edited to add: September 2023 proposals for adding a Symptoms chapter code for Post-exertional malaise to the US's ICD-10-CM.

 

That looks fine as long as the definition is tight enough that everyone is describing the same set of phenomena.

If they're not, it's potentially very unhelpful. We need to know whether PEM (as defined in ME) occurs elsewhere, but a slack definition will result in confusion and lost opportunities.

 

The women (n=1) who RD is referring to in his video is Rachel Riggs. She was all over social media years ago sharing her story about being 'misdiagosed' as having MS. She also has EDS, MCAS ME/CFS et She took Copaxone. She was also on PR for a bit sharing her experience.

https://www.healthrising.org/forums...ltiple-sclerosis-drug-what-does-it-mean.4028/

She has a website about 'clean eating'.

https://www.sandiegouniontribune.co...p-sustain-a-life-and-renew-a-passion-for-food

She also started a fund raiser for her cookbook with 100% royalties donated to the OMF.

https://www.gofundme.com/f/gnf57-cookbook-photography

 

But as far as a I understand PEM is not a recognised symptom of MS, so if you have MS and PEM, another explanation is needed.

I know one person in the UK who is diagnosed with ME and MS. I also heard (from one of the consultants) about someone who was an inpatient at the ME/CFS service in Essex who was re-diagnosed with MS following a brain MRI scan, having been wrongly diagnosed with ME.

 

When I was diagnosed by an M.E specialist with over 20+ yrs experience, who co-authored the draft and original version of the ME/CFS consensus document, he wanted to r/o MS first before diagnosing me with atypical M.E. I saw a neurologist who ordered all sorts of blood work and tests at the hospital. MS was r/o.

Ron Davis is not a clinician and doesn't see patients. He meets them and reads into their experiences, he then makes connections that are just down right spreading misinformation IMO.

 

From Rachel Riggs on PR (non-private thread):

“My response to Copaxone is one of the reasons I knew I DIDN'T have MS.
Copaxone does not improve MS symptoms - its aim is to slow progression and number of new lesions.
I always had a weak diagnosis, I had a couple lesions which disappeared over time. That can happen in people who have migraines.”

This sounds about right. MS patients don’t usually have dramatic responses to Copaxone.

 

Long Covid is probably the same thing as ME/CFS.

 

You're right. This goes to the heart of the problem. He speaks like somebody who doesn't have any contact with clinical reality. And because he has no clinical experience, he has no idea how incorrect the things that he says sound.

 

One of the reasons we **don't know** that 'Long Covid is the probably the same as ME/CFS' is that people who have had ME for more than 5 or so years are being excluded from combined LC and ME research. So reducing the chances of knowledge about developments in ME sufferers over years/decades.

 

The study found that later-presenting patients often had five to 10 years of prodromal symptoms like fatigue and generalized weakness before getting a diagnosis of MS.

“They had been going to doctors for years, but the diagnoses were continually missed,” Zachariah says. “While their MS may not be as aggressive as early presenting patients, and they may not need the same types of medical treatment, we have got to figure out a better way to get answers for these patients who have these nonspecific symptoms.”

It is much easier to get a dx of M.E first if one fits the criteria after six months of PVFS.

 

Was this posted yet? From Invest in ME

https://www.youtube.com/watch?v=ijkCw7VeOLo

 

AI summary of above video

Summary of #IIMEC16 14 Ron Davis 16th Invest in ME Research International ME Conference 2024

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00:00:00 - 00:25:00
In the "#IIMEC16 14 Ron Davis" YouTube video, biochemist Ron Davis discusses various aspects of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). He explores the impact of infections on MFS patients, focusing on mitochondrial fragmentation, oxidative stress, and reduced ATP production.

Davis highlights a study revealing increased oxidative reactions in MFS and Long COVID patients, particularly in females. He also introduces the potential of BH4 as a reducing agent to combat oxidative stress but acknowledges the challenges in studying it due to its sensitivity and low abundance.

Furthermore, Davis delves into the importance of metals like iron, manganese, and copper for various cellular reactions, explaining that their transport into cells requires nitric oxide. However, if the body experiences oxidative stress from infections, it can lower BH4 levels, reducing nitric oxide and limiting essential metals' entry into cells, leading to a sustained illness. He suggests potential solutions, such as protecting BH4 or discovering drugs that produce nitric oxide directly.

Davis also discusses the potential role of herpes viruses, specifically EBV, HHV-6, and CMV, in causing ME/CFS. He explains that these viruses are often found in ME/CFS patients and can cause the condition, with trauma potentially activating them. He suggests that the focus on SARS virus as the cause of ME/CFS may be misplaced and that herpes viruses could be the primary culprits.

Additionally, he discusses ongoing research at the University of Utah aimed at blocking a specific pathway contributing to ME/CFS patients' energy deficiency, with the potential development of FDA-approved drugs or natural products to inhibit this pathway.

• 00:00:00 In this section of the #IIMEC16 conference, Ron Davis discusses the impact of infections on MFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) patients, focusing on mitochondrial fragmentation, oxidative stress, and reduced ATP production. He highlights a study by Vishnu Haran and Mark Davis that revealed increased oxidative reactions in MFS and Long COVID patients, particularly in females. Davis also mentions the potential of a compound called BH4 as a reducing agent to help combat oxidative stress, but acknowledges the challenges in studying it due to its sensitivity and low abundance.

• 00:05:00 In this section of the YouTube video titled "#IIMEC16 14 Ron Davis 16th Invest in ME Research International ME Conference 2024," biochemist Ron Davis discusses the importance of the molecule BH4. BH4 is an essential cofactor involved in various biochemical reactions, including the conversion of fil Alanine to tyrosine, which is used to produce dopamine and serotonin. Additionally, BH4 plays a crucial role in converting Arginine to Citrulline, generating nitric oxide. Nitric oxide is a simple molecule that can diffuse rapidly and go through membranes, making it a useful molecule for regulation. The discovery that a patient with ME/CFS experienced significant improvement after taking a BH4 precursor led researchers to investigate the potential role of BH4 in ME/CFS. They believe that a problem with BH4 could be linked to the observed decrease in dopamine levels. Furthermore, nitric oxide can react with proteins and modify their function, which may be critical in ME/CFS.

• 00:10:00 In this section of the "#IIMEC16 14 Ron Davis" YouTube video, Ron Davis discusses the importance of metals like iron, manganese, and copper for various cellular reactions. He explains that these metals cannot directly enter cells without being transported, and this transport requires a reaction with nitric oxide. However, if the body experiences oxidative stress from infections, it can lower the levels of a compound called BH4, which in turn reduces the amount of nitric oxide and limits the amount of essential metals entering cells. This cycle can lead to a sustained illness as the body continues to produce reactive species and cannot break the cycle. Davis suggests potential solutions, such as finding a way to protect BH4 or discovering drugs that produce nitric oxide directly. He also shares his team's efforts to measure BH4 levels using a high-performance liquid chromatography instrument.

• 00:15:00 In this section of the #IIMEC16 conference by Ron Davis, he discusses the challenges and advancements in measuring and stabilizing Betaine Hydrochloride (bh4) levels in patients' blood samples. The speaker mentions that they have developed a method to quickly analyze bh4 levels using a vacuum-sealed blood tube with added reducing agents. The preliminary results indicate that bh4 levels are approximately 39% of the total (bh4, bh2, bh3) in ME/CFS patients, which is half of the healthy person's total. Additionally, the ratio of bh2 to bh4 seems to be a problem. The team has also discovered that other infections and stressors can activate endogenous EBV and HHV-6, which can replicate and cause symptoms in ME/CFS patients.

• 00:20:00 In this section of the "#IIMEC16 14 Ron Davis" YouTube video, Ron Davis discusses the potential role of herpes viruses, specifically EBV, HHV-6, and Cytomegalovirus (CMV), in causing ME/CFS. Davis explains that these viruses are often found in ME/CFS patients and that they can cause the condition. He also mentions that trauma can activate these viruses and lead to ME/CFS symptoms. Davis suggests that the focus on the SARS virus as the cause of ME/CFS may be misplaced, and that herpes viruses could be the primary culprits. He also explains that when the immune system is activated, an "attack and shunt" pathway is turned on, which reduces ATP production and leads to fatigue. Davis speculates that this pathway may be locked on in ME/CFS patients, possibly due to a persistent immune response.

• 00:25:00 In this section of the #IIMEC16 conference, Ron Davis discusses ongoing research at the University of Utah aimed at blocking a specific pathway that contributes to the energy deficiency experienced by ME/CFS patients. Researchers are developing a FDA-approved drug or natural product to inhibit this pathway. Additionally, they are engineering Zeer fish, which are easy to work with and can be genetically modified, to study the effects of this pathway on their swimming speed. By activating the pathway and observing the fish's slowed swimming, researchers hope to identify methods for unblocking it, potentially leading to effective treatments for ME/CFS. Davis expresses optimism about the progress being made in the field and the timely development of reasonable and potentially great treatments.

 

Ron sounds a bit tired in this video but also optimistic. It’s worth watching.

 

This looked exciting but I watched the corresponding segment and it seems to be that bh4 is 39% in a single mecfs patient, and Ron implies it's a blood relation of his. So sample size not big yet!

The part where teams are genetically engineering zebra fish to overuse the itaconate shunt is interesting! I'm not at all convinced about the itaconate shunt idea but we definitely need to open up the world of animal models. It's the only way to iterate treatments fast. That and the WASF3 mouse models create hope for me.

 

His son, Whitney.

 

Do you have any more info on this? I have heard of the WASF3 finding and the fact the researcher wanted to do a drug trial (als drug?) but not of a mouse model.