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ME-CFS-Autism

Cort

Phoenix Rising Founder
That theory follows some ME/CFS theories almost exactly I would say - a large constellation of problems interact in different ways to cause mitochondrial problems and ultimately cause autism......I have no idea if it's true but the similarity of the approach is striking...
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Hi Crappy, I have refered to CFS as adult onset autism n the past. It is interesting to hear this from the "mainstream" medicos though. There is a lot of biochemistry and symptomology in common, even if you ignore the screaming Tyranosaur in the room, XMRV. Bye, Alex
 

Carrigon

Senior Member
Messages
808
Location
PA, USA
I'm definitely on the autism spectrum. But in my case, I think I got it as a child after the four in one vaccine that almost killed me. I can remember having autism "symptoms" as young as about four years old.
 

richvank

Senior Member
Messages
2,732
Hi, all.

I certainly subscribe to the view that autism and CFS are essentially the same from the basic biochemical standpoint. In fact, that similarity, which I saw in a paper published by S. Jill James et al. in late 2004 is what prompted me to develop the Glutathione Depletion--Methylation Cycle Block hypothesis for the pathogenesis and pathophysiology of CFS, and it is also what formed the basis for selecting treatments directed toward lifting the partial block in the methylation cycle.

I wrote an article that appeared in the Townsend Letter about this similarity.

Note that Dr. Hyman mentioned methylation in his article about autism. He and I were both part of the Ratna Ling Working Groups a couple of years ago, and he was present when I gave a talk on this hypothesis. I have a copy of his book The UltraMind Solution, and I recommend it.

For those interested in more information about this, all of the above and more can be found at www.cfsresearch.org by clicking on CFS/M.E. and then on my name.

Best regards,

Rich
 

redo

Senior Member
Messages
874
I think this CFS-autism link is vital to unraveling what's behind this disease, as the prevalence seems a bit to high to be just coincidental. Looking at my family, there are just so many cases of it. On one of the branches in my family tree, there's almost half who's got some mild form of autism, plus one with utterly severe autism. And I have siblings with some mild, but very noticeable form of autism. And I might even have slight hints of it myself. Both in the ways of very often using the rational part of the brain for understanding social interaction (and not going with the gut/intuition which is normal). And when I was healthy, I had a photographic memory and excelled in science and maths, but some parts of understanding body language could have gone somewhat quicker. Lots of small cues really, but I don't come across as having ASD for outsiders (and nor do I qualify for it), but it might be that I really have some hints of it, but compensate, so what's really a very light case comes across as totally normal. I am guessing when we find out what's behind the diseases, maybe a long time from now, we'll see that there are some big overlaps in etiology for parts of the ASD group and CFS.
 
Messages
11
I have been using alot of the autism research, studies and treatment to better understand cfs. They do have the same similarities in alot of ways, just that autism is address at the youth stage and cfs is an adult stage. I kind of see the stress put on the body caused by autism may effectively wear out and fatigue systems resulting in mitochondrial and methylation disfunctions. Just another opinion though.
 

taniaaust1

Senior Member
Messages
13,054
Location
Sth Australia
The side of my family (my fathers side) which tends to get CFS and ME ... also is the same side as which I get my Aspergers from...
also FM on that side of the family too (dads mother) without CFS going on with it.

(celiac disease, rheumatoid arthritis and also a extremely rare autoimmune disease is all on that side of my family).

I had Aspergers since I was a baby. My daughter who was NEVER vaccinated, has it too.
 

SilverbladeTE

Senior Member
Messages
3,043
Location
Somewhere near Glasgow, Scotland
The side of my family (my fathers side) which tends to get CFS and ME ... also is the same side as which I get my Aspergers from...
also FM on that side of the family too (dads mother) without CFS going on with it.

(celiac disease, rheumatoid arthritis and also a extremely rare autoimmune disease is all on that side of my family).

I had Aspergers since I was a baby. My daughter who was NEVER vaccinated, has it too.

taniaa,
well, about everyone's ingesting mercury and organophosphates and other horrible poisons in our food, air and water :/
I live right next to one of the most polluted sites in Europe, seen whole families wiped out by cancer etc. While they spend 100 MILLION to clean the industrial site up so they could build house on it ot make "phat-lewt" ...they spent NOTHING on researching or even caring about the huge incidences of ill health here. As one GP said, he'd never seen rates of chronic and terminal illnesses like he has here.
All about $$$ in the end, I don't trust any damn study the government, vaccine or any other industry puts out in such areas, because much of the time, they LIE to cover their arses :(
See the PACE trial in regards ot ME, for bullshit, do folks think it's any different when it comes to other areas? :/
 

shannah

Senior Member
Messages
1,429
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redo

Senior Member
Messages
874
I just took this, and I scored 1.4 lower than the average score (32 or higher indicates ASD), but despite that, I do have some very slight hints of it.
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
Apologies for the length of this post.

I'm constantly surprised why a similar study isn't done for ME/CFS rather than virus hunting or childhood trauma at either end of the dichotomy. After all 'fatigue' is an energy deficit by another name. There are also many similarities between autism and ME/CFS symptoms and quite a lot of converging evidence for both conditions.

Its worthwhile reading the full paper referenced in the Huff post article.

A few things struck me :


They only needed 10 patients and controls to show statistically significant differences in this preliminary study;

One objection to mito studies in ME/CFS is the need to carry out muscle biopsies which is costly; invasive and also appears to be based on the assumption that any deficit will be found in skeletal muscle. To quote the autism paper :

Mitochondrial function in disease often has been investigated in muscle biopsies6; however, the detection of mitochondrial defects in readily available cells from body fluids (lymphocytes and platelets7?) would be valuable under the assumption that many such defects may not be confined to muscle or the brain, tissues in which mitochondrial diseases are most strongly evident

Clearly there are other ways to more easily study a systemic mitochondrial deficit;

another quote :

The lactate-to-pyruvate ratio reflects the redox state of the cytosolic compartment,28 such that a lactate-to-pyruvate ratio of 12 (as in controls) indicates a ratio of oxidized NADH to reduced NADH of 750:1 and a lactate-to-pyruvate ratio of 6 (as in autism) indicates a ratio of oxidized NADH to reduced NADH of 1500:1. This more oxidized cytosolic redox state in autism could favor anaerobic glycolysis over oxidative phosphorylation as a source of adenosine triphosphate.28? Although skeletal muscle can tolerate this shift in metabolism, consequences for brain function could be devastating due to its heavy reliance on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes.7,29

Accepting that muscles may not be the best place to look, physiological muscle abnormalities have indeed been found in ME/CFS using biopsies.

e.g. Lane et al found :

Muscle histometry in patients with chronic fatigue syndrome generally did not show the changes expected as a result of inactivity. However, patients with abnormal lactate responses to exercise had a significantly lower proportion of mitochondria rich type 1 muscle fibres.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2169994/pdf/v064p00362.pdf

They also found evidence of hypertrophy of type II (fast twitch) muscle fibres.

In other words, the proportion and size of muscle fibres in some ME/CFS patients (an Oxford defined cohort) showed a switch from the mitochondria rich endurance related type I fibres to anaerobic type II fibres. Its logical to infer, as is suggested with autism, that this compensatory switch to pathways that utilise anaerobic glycolisis results from a mitochondrial deficit and again, as in autism, would have severe implications for proper brain functioning. Its also interesting to note how muscle fibre hypertrophy occurs (as in bodybuilding) hypertrophy occurs when existing muscle is unable to meet the energetic demands put on it.

********************

Sensory gating deficits occur when the brain is unable to filter out common repeated innocuous signals leading to various types of 'sensory overload'. Sensory gating deficits are suspected of playing a role in autism, schizophrenia; fibromyalgia and one dissertation showed a weak association with ME/CFS (but using a not necessarily relevant stimulus).

Sensory gating deficits could underlie sensory integration problems; hallucinations; diffuse pain and PEM respectively in each of these conditions.

In the context of a mitochondrial deficit, its interesting that glutathione depletion is associated with a sensory gating deficit in schizophrenia.

*******************

Finally gut problems. Here's a quote from an old review paper on glutathione deficiency in human disease. A lot of available glutathione is lost through the gut.

The cellular stores of glutathione can also be depleted through the glutathione transferase reaction in which a glutathione molecule is conjugated to foreign compounds. This GSH complex is then excreted resulting in a loss of cellular GSH ....and there is evidence that this system is important in the gastrointestinal mucosa as a means to detoxify compounds present in the bowel lumen

http://www.glutathioneexperts.com/pdfs/glutathione-neurodegenerative-3.pdf

Could this be the link between bowel issues/pathogens in autism and ME/CFS? Is cellular glutathione being depleted in neutralising gut toxins or is it the case that glutathione depletion results in impaired defences against gut toxins resulting in IBS like symptoms?

In this context, its also interesting that Maes has shown that a combination of zinc and acetylcysteine (a glutathione precursor) can normalise leaky gut in ME/CFS patients.

http://www.ncbi.nlm.nih.gov/pubmed/19112401

**************************

For what its worth my wife and I took the autism spectrum test. My wife (who doesn't have ME/CFS) scored 12 and wasn't in the least surprised when I scored 38 (and wondered if this was a record).:D
 

richvank

Senior Member
Messages
2,732
Hi, Marco.

With respect to glutathione in ME/CFS, if you haven't viewed the video or checked the slides from my recent seminar in Sweden, I suggest that you take a look at them, here:

http://iaomt.media.fnf.nu/2/skovde_2011_me_kroniskt_trotthetssyndrom/$%7Bweburl%7D

Best regards,

Rich
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
Hi, Marco.

With respect to glutathione in ME/CFS, if you haven't viewed the video or checked the slides from my recent seminar in Sweden, I suggest that you take a look at them, here:

http://iaomt.media.fnf.nu/2/skovde_2011_me_kroniskt_trotthetssyndrom/$%7Bweburl%7D

Best regards,

Rich

Hi Rich

Thanks I will when I get the chance.

I also appreciate that glutathione depletion has been a major element in your methylathion hypothesis for a long time.

I'm afraid I'm one of those people that has to work things out for themselves (slowly) before I can fully accept them. Possibly another trait on the ASD spectrum?

PS - Forgot to ask. Has a sensory gating deficit figured in your model?
 

Battery Muncher

Senior Member
Messages
620
Apologies for the length of this post....[]

Don't apologise, that was a very interesting post!

I found this thread fascinating because, like many people here, I've also seen a lot of personality changes. I have definitely 'become' more autistic in behaviour. I used be very sociable but am now much more interested in things and numbers. I can no longer function in social situations.

I also found the information about type II muscle fibres interesting. Before I came down with ME/CFS, I was a very fast sprinter, one of the best in the region. Yet, I had never shown any real athletic prowess previous to that. A lot of people who knew me found that baffling. Maybe that's a tenuous connection, but it got me thinking.
 

mellster

Marco
Messages
805
Location
San Francisco
Similar here - I've done well in a lot of sports, have always been sporty but never reached athletic prowess either, I was a decent sprinter (for my very long legs) and during the course of this journey I have never significantly lost muscle mass, i.e. I feel I have had a type II muscle fibre "shift" (with onset of some muscle twitching) during practising martial arts, but aerobic exercise has become quite challenging. Also, presonality-wise, I have definitely shifted towards the autistic spectrum. While I can function in social situation, I don't enjoy them much anymore and avoid them. But this has definitely also to do with the onset of FM symptoms and gut/inflammatory issues, which just makes it hard to go out of your comfort zone. I bet the link from Autism to physical illness/disorder will eventually be proven beyond doubt ;) cheers

Don't apologise, that was a very interesting post!

I found this thread fascinating because, like many people here, I've also seen a lot of personality changes. I have definitely 'become' more autistic in behaviour. I used be very sociable but am now much more interested in things and numbers. I can no longer function in social situations.

I also found the information about type II muscle fibres interesting. Before I came down with ME/CFS, I was a very fast sprinter, one of the best in the region. Yet, I had never shown any real athletic prowess previous to that. A lot of people who knew me found that baffling. Maybe that's a tenuous connection, but it got me thinking.
 

richvank

Senior Member
Messages
2,732
Hi Rich

Thanks I will when I get the chance.

I also appreciate that glutathione depletion has been a major element in your methylathion hypothesis for a long time.

I'm afraid I'm one of those people that has to work things out for themselves (slowly) before I can fully accept them. Possibly another trait on the ASD spectrum?

PS - Forgot to ask. Has a sensory gating deficit figured in your model?

Hi, Marco.

Fair enough! I'm kind of that way, myself!

I haven't looked into sensory gating, so I don't know what that is all about.

Best regards,

Rich
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
Hi again Rich

I'm sure something like sensory gating may seem a little left field compared to mito/immune issues but I'll try to explain how I think it may be relevant.

Sensory gating basically refers to the mechanism by which we separate 'signal' from 'noise'. Our nervous system (I would tend to include the immune system in this) is constantly being bombarded by information from all the senses and its obviously a biological imperative to be able to separate out those signals that are important and suggest danger from those that are habitual and innocuous. Take the startle reflex. A sudden sharp noise will make you jump and your heart race. If the same noise continues with no associated danger then normally it becomes just more background noise and we become habituated to it. Similarly a sudden sharp pain might suggest an injury but you wouldn't want to be aware 24 hours a day that you are wearing a watch or that your shoes pinch a little. Normally these innocuous sensations are habituated and treated as unimportant background noise.

Problems come when there is a sensory processing deficit (which is a fairly easy thing to test experimentally using a paired response paradigm to determine the degree to which the nervous system is able to habituate 'harmless' stimuli).

In the past, a certain Dr Goldstein has suggested sensory gating as the mechanism underlying ME/CFS. I'm not suggesting this as an alternative explanation to your own model but as an adjunct that might help explain some of our more bizarre symptoms. I have to admit to being frustrated sometimes by 'black box' explanations that a retrovirus or mitochondrial deficit can cause all of our physical and neurological symptoms without describing the mechanism. I suggesting that a sensory gating deficit may be such a mechanism.

I admit that I take a broad brush approach trying to reconcile various parts of the elephant so to speak. What struck me is that certain diseases/conditions where a sensory gating deficit has been shown (Schizophrenia; Altzheimers; bipolar disorder; fibromyalgia and of course autism) are ones where a glutathione deficit has also been shown. I'd suggest that there is very strong evidence that there is also a mitochondrial deficit in ME/CFS but that to date a sensory processing deficit hasn't been investigated beyond one small dissertation trial.

Of course a correlation between a sensory gating deficit and a glutathione deficit may be just that but there is evidence to suggest that they are causally linked.

For example experimentally induced damage to mitochondria alters the 'startle reflex' :

http://www.sciencedirect.com/science/article/pii/S0304394097004825

glutathione depletion can be shown to directly affect sensory gating in schizophrenia :

http://www.bioportfolio.com/resourc...Drug-Treatment-In-Prepulse-Inhibition-In.html

and glutathione supplementation can relieve some symptoms of schizophrenia :

http://www.ncbi.nlm.nih.gov/pubmed/18436195


Looking at how the sensory gating deficit manifests itself in these conditions is also suggestive. In autism there are the familiar problems of problems with sensory integration; overload phenomena etc. In schizophrenia, the inability to 'gate' sensory input leads to auditory and other hallucinations and of course in fibromyalgia you have the constant diffuse pain and fatigue.

Look then at our common symptoms : fatigue; pain; IBS; sensitivity to light and noise; feeling 'tired but wired'; food and chemical sensitivities. All could be easily explained if a sensory gating deficit means we are unable to screen out ongoing sensations. Some time ago I even initiated a thread of my clothes sensitivity that seemed to ring a bell with many members.

Its also easy to hypothesise that this constant bombardment of sensory input might overwhelm the nervous system resulting in brain fog; problems with multitasking; 'fatigue' and PEM.

I should add that I'm not suggesting that these sensations are 'illusory' or that we are just abnormally sensitive to pain for example. From my own experience, if I hit my thumb with a hammer it still hurts but no more than previously. On the other hand I can't sit still comfortably for any length of time as muscle and joint pain increases over time rather than habituating. I also don't rule out the possibility that a mitochondrial deficit may be causing for example leaky gut or microtrauma to muscles but that a sensory gating deficit would also accentuate the perception of it.

As I said, I tend to look at these things from a broad brush perspective as I don't have the biochemistry background and I can't explain exactly how a mitochondrial deficit and sensory processing deficit might be linked.

This blogger has had a go however :

http://bb-cfs.blogspot.com/2011/05/your-brain-on-atp-purinergic-signalling.html

it appears that ATP is the chemical messenger for the purinergic system (remember the Lights?) and this blog suggests that low ATP could result in a 'depression' of neural activity and hence brain fog etc.

I'd suggest that ATP also plays a key role in opening and closing the 'gates' that control sensory inputs in the purinergic system and that low ATP results in inadequate inhibition/habituation and thus a sensory gating deficit.