Why does Kenny De Meirleir diagnose almost every patient with bacterial infections?

[duncan]

I don't think anyone is arguing that chronic infection cannot exist but rather that the evidence for it playing a major role in ME/CFS just isn't there.

I'm not sure how meaningful this argument ultimately is. I can think of at least two major pathogens - enteroviruses and Borrelia - that can explain, at least in part, most ME/CFS symptom clusters. But conventional testing is frequently inadequate for such illnesses. It is woefully easy to take a Lyme patient who one day tests only 4 IgG bands positive and have an ID or rheumotologist claim she cannot have Lyme; she must have ME/CFS - and then have her Bb values shoot up to 6 bands the next month. Multiply that by tens of thousands of patients, and there's potentially a problem that is rooted in testing short-falls.

So, to declare we cannot see a pathogen when testing pwME might simply be stating an obvious problem even when a pathogen is responsible.

This is not to say ME/CFS is not an autoimmune disorder, or some sort of gross immune disruption. It is just pointing out we are no where near the point where we can confidently rule out all pathogens.

 

[Learner1]

These citations are not serious science. We have no reliable evidence for anything wrong with mitochondria in ME. I think we can say that quite clearly. There might turn out to be but my point about being dead was a direct quote from Mike Murphy who is a mitochondrial expert at Cambridge who was invited to talk at an IiME conference a year or two ago. The symptoms of ME do not sound remotely like under performing mitochondria. Murphy was quite clear about that. It is possible that mitochondria harbour signalling molecules involved in generating symptoms but that would be quite separate from an 'energy deficit' which I think is a misconception.

I have looked after many people with failing energy supplies due to a range of illnesses and their condition does not remotely resemble ME.

After sitting through 4 days of researchers lecturing to doctors at a major mitochondrial disease conference last year, it was clear that there's a lot that can go wrong with mitochondria.

Dr. Naviaux spoke on the environmental impacts to mitochondria, warning the doctors about exposure to environmental toxins and pharmaceutical drugs.

And the graphs they were showing looked an awful lot like those that McLaren and Myhill have published.

Some of us may have primary mitochondrial disease. The number of genes linked to it has been steadily growing over the past few years.

However, it's more likely that the rest of us have environmental factors impacting our mitochondria as Naviaux discussed. Most diseases of aging have damaged mitochondria, it happens over time due to the environmental factors we've encountered through our lives. Toxins get into our mitochondria and impact the efficiency of ATP production.

Another supplement I didn't mention before that gives me direct benefit, and I know others here benefit from it too, is Enada NADH, and others have found help from nicotinamide riboside. Both directly assist ATP production in the mitochondria.

 

[sb4]

Doug Wallace thinks around 80% of disease is due to mitochondria heteroplasmy, the rest is due to faults in the nuclear DNA. So it could well be that a virus is keeping our mito down, or causes immune problems which effect our mito, or something kicks off CFS and sends us in to a downward spiral affecting our mito, or something else.

I think you would need to remove the offending agent then put the mito in an enviroment where they can repair / function correctly. Maybe if we do enough for the mito then we can beat it without removing the offened agent, if it is even still there.

 

[Learner1]

Doug Wallace thinks around 80% of disease is due to mitochondria heteroplasmy, the rest is due to faults in the nuclear DNA. So it could well be that a virus is keeping our mito down, or causes immune problems which effect our mito, or something kicks off CFS and sends us in to a downward spiral affecting our mito, or something else.

I think you would need to remove the offending agent then put the mito in an enviroment where they can repair / function correctly. Maybe if we do enough for the mito then we can beat it without removing the offened agent, if it is even still there.

I think this is an interesting discussion.

From what I've gathered from Naviaux's presentations and in talking with him directly, removing the offending agent, then repairing the damage/rebalancing the biochemical processes would be the ideal.

Two good things about mitochondria - they die and are reformed every so often, so there's the opportunity to change bad ones to goid ones, and one can encourage the proliferation of more, through exercise and other interventions. More mitochondria means more capacity to make ATP.

One question that comes up is if mitochondria are compromused, is pushing them to make more ATP faster a good thing, or a potentially damaging thing? Or, is it best to fix them, by giving them good nutrients they need, before pushing them to do more?

I'd like to know the answer. I find that sublingual NADH gives me an energy boost within 15 minutes, but try to save it for when I really need it, not knowing the answer.

Also, I found the attached paper which has some interesting ideas about attacking Alzheimer's from a mitochondrial perspective...and recognized some familiar interventions. I suspect (and have already experienced) there's a lot that can be done yo optimize mitochondrial function to help us.

The question is how best to go about it.

 

[Twazzle]

As we have learned with the PACE/CBT/GET story, a lot of unreliable evidence doesn't add up to reliable evidence. I don't think anyone is arguing that chronic infection cannot exist but rather that the evidence for it playing a major role in ME/CFS just isn't there.

Just to be absolutely clear - KDM does not believe that active bacterial infections are causing ME, nor does he treat them in the majority of his patients like you suggested in the title of the thread. The question has been explicitly answered.

I summarised his approach in an earlier post. Obviously if he does find an bacterial infection that needs treating, and only if the testing confirms so, he will treat as any other doctor would. However this is in the minority of patients.

 

[justy]

The symptoms of ME do not sound remotely like under performing mitochondria.

Really? I had 20 symptoms from a list of possible symptoms of mitochondrial disease, which are:

Fatigue
respiratory problems
Ptosis
hearing loss
Vision problems (which may come and go)
cardiac issues
weakness
cramps
gastrointestinal issues
Gastro oesophageal reflux
irritable bowel
constipation
diarrhoea
neuropathic pain
Dysautonomia
temperature instability
migraines
seizures
dementia
neuropsychiatric disturbances.

source:

https://www.umdf.org/what-is-mitochondrial-disease/possible-symptoms/

who themselves say that mitochondrial disease of adult onset can present with:

Systemic: CFS-like illness (Chronic Fatigue Syndrome – like illness)

I would be interested to see your list of M.E symptoms so I can see what you yourself are comparing mito disease to.

 

[sb4]

@Learner1 I am very interested in improving mito. Have you tried the ALCAR and R-Lipoic Acid from that first paper you linked?

You may also be interested in using methylene blue and red/IR light to enhance mito function. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428125/). The methylene blue I can't handle due to tachycardia but it works by donating electrons to the ECT and it absorbs red light. The red light knocks off NO from cytochrome C Oxidase so oxygen can take it's place, I also suspect it does much more than this to increase ATP. I have benefited from red light, it can penetrate 10-30cms so it can get almost everywhere including brain. Of course for most of our evolution we would have got plenty of this light via the sun.

Also I have heard melatonin is massively important for repairing mito and keeping them healthy. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3100547/) (https://www.ncbi.nlm.nih.gov/pubmed/28118492). I have heard it's not a good idea to take melatonin, something to do with feedback systems. So the best way to increase it would be to avoid blue light, particularly at night, and increase UVA exposure to eyes (http://www.sciencedirect.com/science/article/pii/S1532045611001517). This could be achieved by being outdoors all day.

I have had moderate success with these things however live at 53rd latitude so not an ideal test case.

 

[Alvin2]

Not that i'm endorsing this misguided exercise but PQQ increases synthesis of mitochondria iirc

 

[Learner1]

@Learner1 I am very interested in improving mito. Have you tried the ALCAR and R-Lipoic Acid from that first paper you linked?

Yes to both. Especially with alpha lipoic acid. I use oral and IV PolyMVA. The IVs give me a burst of energy.

You may also be interested in using methylene blue and red/IR light to enhance mito function....

Interesting. I'll look into it.

Also I have heard melatonin is massively important for repairing mito and keeping them healthy. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3100547/) (https://www.ncbi.nlm.nih.gov/pubmed/28118492). I have heard it's not a good idea to take melatonin, something to do with feedback systems. So the best way to increase it would be to avoid blue light, particularly at night, and increase UVA exposure to eyes (http://www.sciencedirect.com/science/article/pii/S1532045611001517). This could be achieved by being outdoors all day.

Melatonin interacts with the immune and endocrine systems. It should be taken under a doctor's supervision - there are pros and cons, and you should take the correct dosage for you. I originally took high doses during my cancer treatment and currently take it for its immune system properties.

I have had moderate success with these things however live at 53rd latitude so not an ideal test case.

Many of these things can help. It's good to be under a doctor's guidance to ensure what we're taking is compatible and dosage is correct.

@Alvin2 I've tried PQQ but didn't see a benefit. It sounds good on paper. Same with MitoQ, which I also heard good things about but didn't see a benefit worth the price.

Exercise can also promote synthesis of mitochondria (provided we do it within our energy envelope and avoid PEM) and it's cheaper.

If we take things that interfere with our functioning or harm us, I'd say that's misguided. But trying things that have been researched and have been shown to have beneficial qualities may just be worth a try.

I've benefited a lot from non-drug interventions and would be far sicker and less functional had I not tried them. I don't run off and try everything, but its wise to research any new idea, look at the risks and benefits, and discuss with one's doctor before carefully selecting which interventions to try in what dose, and also what time of day to try them, which can sometimes make a significant difference.

 

[sb4]

Melatonin interacts with the immune and endocrine systems. It should be taken under a doctor's supervision - there are pros and cons, and you should take the correct dosage for you. I originally took high doses during my cancer treatment and currently take it for its immune system properties.

Yes I have heard bad things about melatonin so don't take it. I have anecdotal good melatonin response (better sleep) from sun gazing, ie uv light in the eye however of course you have to be careful with this, and it's difficult to do at high latitudes.

 

[msf]

I do not think this is a realistic assessment, Valentijn. If this is standard practice then every other physician would do the same and people would not travel thousands of miles.

Nope, because most physicians do not know the first thing about how to test for Yersinia, never mind how to treat it.

 

[msf]

As we have learned with the PACE/CBT/GET story, a lot of unreliable evidence doesn't add up to reliable evidence. I don't think anyone is arguing that chronic infection cannot exist but rather that the evidence for it playing a major role in ME/CFS just isn't there.

Can I just point out that now me and AB are the ones who are on-topic?

Note to future moderator - it may help people looking up stuff if the posts about mitochondria are moved to a different thread.

 

[justy]

Can I just point out that now me and AB are the ones who are on-topic?

Note to future moderator - it may help people looking up stuff if the posts about mitochondria are moved to a different thread.

Can you report the issue?

 

[msf]

I´ll try, but contrary to a certain person´s allegations, I have never reported something to a moderator before - did you say there is a report button somewhere? Also, do we actually have a moderator now?

 

[Learner1]

I´ll try, but contrary to a certain person´s allegations, I have never reported something to a moderator before - did you say there is a report button somewhere? Also, do we actually have a moderator now?

So sorry to have derailed your post. I have no idea how to move anything but go ahead and do so.

 

[sb4]

I apologies for derailing this thread however we have stopped posting about it now and it was only like 6 posts in a thread of 200+. Does it really need reporting and moving to a different thread?

 

[msf]

I apologies for derailing this thread however we have stopped posting about it now and it was only like 6 posts in a thread of 200+. Does it really need reporting and moving to a different thread?

I don´t think it did, but now you have questioned whether it does, and I have replied to it, it definitely does now.

Just kidding, I didn´t realise that people were done with mitchondrial stuff.

 

[CFS_for_19_years]

And now I'm responding to an off-topic question so that ivorin gets an answer:

Do you have any links as to the sustained remission rates of responders from phases 1 and 2? I'm not dissing, I'm genuinely interested to find the numbers.

Any remission rates would be included in the articles below. That's all we know so far.

Benefit from B-Lymphocyte Depletion Using the Anti-CD20 Antibody Rituximab in Chronic Fatigue Syndrome. A Double-Blind and Placebo-Controlled Study
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0026358

B-Lymphocyte Depletion in Myalgic Encephalopathy/ Chronic Fatigue Syndrome. An Open-Label Phase II Study with Rituximab Maintenance Treatment
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488509/

 

[ivorin]

And now I'm responding to an off-topic question so that ivorin gets an answer:

Any remission rates would be included in the articles below. That's all we know so far.

Benefit from B-Lymphocyte Depletion Using the Anti-CD20 Antibody Rituximab in Chronic Fatigue Syndrome. A Double-Blind and Placebo-Controlled Study
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0026358

B-Lymphocyte Depletion in Myalgic Encephalopathy/ Chronic Fatigue Syndrome. An Open-Label Phase II Study with Rituximab Maintenance Treatment
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488509/

Cheers for this, almost the numbers I was looking for <3