CDC - Allostatic load - nervous system?

[William Holder]

Several years ago the CDC conducted a study suggesting a gene within our nervous system that regulates our reaction to stress was damaged in people with CFS.
This was the first thing I ever read about CFS that made sense and could account for the wide diversity of individuals impacted by this illness.
Now that the excitement over xmrv has come and gone - is any research still exploring this potential cause of CFS?

 

[Marco]

Hello William

As possibly a member of a sub-set of PWME who does react badly to stress, plus the fact that stress does exacerbate the symptoms of ME/CFS (and other neurological illnesses) I've certainly no objections to the line of research.

Given the CDC's approach to cohorts thought its difficult to know if they were onto something or it was just an artefact of lax criteria.

It seems the concept of allostasis and allostatic load is alive and well generally as a concept but that it had lost traction with repect to ME/CFS.

ME/CFS research appears to me to have moved on from the concept of stress, in its modern interpretation as psychological stress, precipitating and maintaining the illness through adding to allostatic load and its physiological consequences to more of Selye's original concept of stress as any psychological, physiological or pathological stressor.

This wider concept of a range of potential stressors leading to an overload of the body's antioxidant defenses, oxidative stress and systemic inflammation appears to underlie many current models.

A genetic predisposition to stress and an impaired antioxidant response coupled with a range of potential environmental stressors may all contribute to the 'state' of ME/CFS.

I have my own theory why we seem to suffer from many forms of 'overload'.

That's my current take on it anyway.

 

[Enid]

I think ME research happily has moved a long way from the concept of stress as psycholgical in origin or maintaining. Something clung to in the UK in particular and which research findings/pathologies now long dismissed.

 

[William Holder]

Thank you for taking the time to respond.
In my time with CFS (17 years), it is clear to me I am easily stressed mentally and that this stress is tremendously debilitating. I am also impacted by PEM and this may disable me for a period of time but is hardly as impactful.
An argument, a long excited conversation, anticipating some event or falling behind in my very limited obligations can wipe me out just as easily. Because these are really just simple everyday events I'm constantly fatigued. PEM in a way offers me a little relief since I feel more comfortable about having gotten something done or exercising.
I can't get away from feeling that I am genetically damaged and that I was predisposed to this damage.

 

[maryb]

William this happens a lot with many people with ME, its a physical response due to the illness, nothing to do with psychology. I read somewhere - sorry don't know where that something is damaged that produces this reaction. Someone with more brain cells may be able to elaborate
I totally get where you are coming from, in my job before ME I did battle with NHS consultants,chair of PCTs etc. after becoming ill when I was at my worse I couldn't even make a phone call to the bank. Like you now I couldn't even contemplate having an argument I know what it does to me. We'll get the bigger picture hopefully sometime soon.

 

[sianrecovery]

all sorts of polymorphisms could contribute to these effects, and I think they also fit with the 'canary' concepts of some PWME having poor (er) systems when it comes to processing bio and chemical toxins, hence being particularly vulnerable to the march of modernisation. These weaknesses could exacerbate any immune insult, creating a vicious circle of badly functioning metabolism hampered by uncleared viruses/bacteria etc. In a model like that, the distinction between mental and physical becomes increasingly unhelpful - its all takes metabolic energy. People with long term inflamatory conditions would be especially prone to the snowball effect of down regulated metabolism, poor clearance of toxins, immune dysregualtion, and onward to consistent and repeated episodes of flared 'allergy' type responses to comparatively innocuous substances

 

[alex3619]

One of the problems in discussing stress is the popular notion that stress must be mental. If you kick your toe, sure there may be mental stress, but there is also physical stress to the toe which may initiate inflammatory processes to try to deal with potential infection. Stress is often physical, and indeed I would argue that most stress is physical.

The CDC looked at a small number of genes based on an hypothesis. They did so for a poorly defined patient cohort. Its hard to say what implications this has.

If you had heart disease or MS or TB it is likely that stress would have a negative impact. This would not make heart disease, MS or TB a mental issue. The stressor causes very physical changes to hormones and the immune system. These are at the heart of what stress is.

Bye, Alex

 

[William Holder]

I truly appreciate your responses. I have followed the news here for many years but have not entered into a discussion because - well because it's so powerful emotionally to talk to others who understand instead of loosing all contact with the world and life I once knew and this slow descent into nothing.

 

[richvank]

Hi, William and the group.

For what it's worth, the current version of the Glutathione Depletion--Methylation Cycle Block (GD-MCB) hypothesis still maintains that stressors in the larger sense (including physical, chemical, biological and psychological/emotional stressors) together with a genetic predisposition (at least in the sporadic cases) are responsible for the onset of ME/CFS. Part of the body's response to all these types of stressors is the nonspecific stress response, which involves secreting cortisol, epinephrine, and norepinephrine, and ultimately all these types of stressors place demands on glutathione, which is tied to B12 metabolism, and which in turn is tied to methylation and the folate metabolism in a tight cause and effect sequence. The mix of types of stressors varies from one case to another, but all of them can and do contribute to the onset of cases of ME/CFS in this model.

Best regards,

Rich

 

[sianrecovery]

Rich, do you see porphyria or HPU as particular players in the predisposing factors underlying methylation blocks?

 

[richvank]

Hi, sian.

I haven't received much data on this. Dr. Klinghardt says he sees a lot of HPU (KPU). As you probably know, HPU causes depletion of several nutrients, including B6, zinc, manganese, biotin and others. Some of these are needed as cofactors by enyzmes in the methylation cycle and related pathways. If they are depleted, I would indeed expect that to impact methylation negatively.

When PWMEs write to me reporting that the methylation protocol didn't help them, I usually suggest that they do some testing to see if there are deficiencies in some of the essential nutrients. If zinc and B6 are both low, I suspect HPU.

It would be great to see a study performed in which both the methylation pathways panel and the HPU test were run on the people. Then we could see how prevalent this situation is. But getting funding for that would be difficult, since there are no patentable drugs involved.

Best regards,

Rich

 

[Firestormm]

Allostatic overload in ME/CFS hypothesis published 15 July 2013

I shall post as a thread if it hasn't already been done

Edit: New thread.