Onset associated with Exercise ?

[MeSci]

What I would like to know of every visitor to this thread is, at precisely what point do you believe that your exercise aversion started, and what do you think brought it about? I am sure we would all welcome the opportunity of discussing this in detail with Trudie Chalder to enable her to explain to us just where we went wrong.

You can pass on my answer to Ms Chalder - it hasn't started. When should I expect it to start?

 

[SOC]

You can pass on my answer to Ms Chalder - it hasn't started. When should I expect it to start?

Same here. I'm not averse to exercise. As soon as my body could handle it, I started exercising (mildly) again and I enjoy it. I'll be happy to tell Ms Chalder when my exercise aversion begins... if it ever does. I'm sure she'll be happy to tell me exactly what I'm doing wrong if that time ever comes.

 

[MeSci]

You will often encounter references to Professor Simon Wessely

Have you no respect? You forgot the 'Sir'. This man, clearly The Messiah for millions of sick people (or people who think that they are sick - poor fools), received a knighthood...

 

[Chrisb]

Have you no respect? You forgot the 'Sir'. This man, clearly The Messiah for millions of sick people (or people who think that they are sick - poor fools), received a knighthood...

Let those who give titles to people use them as terms of address.

I have no end of amusement over the term Professor. In addition to the definitions one would expect for those whom we respect, my dictionary includes charlatan and dancing master. It's a sad life.

 

[MeSci]

I don't have PEM fatigue, though or any other time. That part still really puzzles me.

Are you sure? For some of us, PEM doesn't rear its ugly head until 2, 3 or more days after the exhaustion. That's a major reason why it can be so hard to make the connection. My delay is typically 2 days, and between the exertion and the PEM onset I feel quite well and energetic.

 

[Pyr2]

I am really starting to wonder. For a long time I've been denying ME/CFS b/c I have some autoimmune markers (low c4, c3; anticardiolipin, antithryoglobulin antibodies)- Ive been saying to myself, no there is a medically accepted disease there that dr's aren't finding. Now, years later, tests later, Im starting to wonder. In fact, I just came from a store. I used to be the expert shopper. I went in and immediately felt shaky and overloaded. That scared the heck out of me. Same thing with conversations. I had parent teacher night last night and was overloaded by all the talking to the point of getting dizzy and anxious by it all. In other threads I just revealed that I have just been diagnosed with autonomic dysfunction. So it is the AD? Is it the CFS/ME? Is it some unnamed autoimmune disease? Is it my reactivated EBV? I have no idea what to believe but Im scared thats somethings really wrong with not my body so much as a my brain.

 

[Griffin]

Whatever the mechanism I tend to think there's a genetic element along the lines of: have this gene and it makes the catalyst (whatever) more likely to turn into ME. i.e it would be a risk factor.

I had EBV in my 40's, I was very ill, and basically never recovered although not formally diagnosed until cancer made my symptoms far worse. My sister had EBV also in her 40's but after a week or so was up and about back to normal. This is what leads me to a genetic link.

However, I don't believe, I just wonder. Evidence is needed.

 

[MeSci]

This is interesting - I have a similar story. I cycled 700k in 5 days and it took me about a month to recover . Just fatigue though. This was over a year ago and I recovered fully. However my real onset with more symptoms began this year after a particularly tough week on the bike. Now I have full blown ME/CFS.

Often wonder if there was a link to the previous fatigue it not. It could be just cycling that much caused the body to fatigue, and it's totally unrelated. Certainly if this is an immune system disease or autoimmune then its difficult to see how it could lurk around waiting for exertion... But I have no idea

My foggy brain has just remembered a paper cited in my own blogpost! Briefly - if ME is due to leaky gut, anything that can cause leaky gut could theoretically cause ME. I believe that this includes over-exertion, psychological stress, vaccination, infection, toxins, physical injury, food intolerance, etc. But as others have noted, there needs to be something else, otherwise everyone who has over-exerted would have/get ME. So people need to be susceptible to leaky gut, presumably.

But not everyone with ME has/has had leaky gut, so we have to fall back on the multiple-types-of-ME approach, as has been discussed on at least two threads, here and here.

 

[MeSci]

Yes, that patient was Dr John Chia's son, Andrew Chia, who went into remission from ME/CFS after interferon therapy for enterovirus-associated ME/CFS. This was during the time when Dr Chia was trialling interferon treatment for his ME/CFS patients.

I would have thought that interferon was an unsuitable treatment for ME. Maybe it induces a 'false recovery' in a similar way to some other unsuitable treatments, but it also affects the conversion of tryptophan in the gut, increasing the conversion to kynurenine instead of serotonin (which has numerous roles, I believe). So in the longer term it would seem likely to have adverse effects.

If you do a search using the top-right box for 'interferon kynurenine' you will find several threads of interest.

 

[MeSci]

If we're talking a single cause for ME/CFS, we are going to have to find something we are doing (or that happened to us) that people who remained healthy did not do. Millions of people worldwide are exercising at a high level and not getting ME. So exercise is not causal in and of itself. The same is true for infections like EBV. Millions of people get EBV, relatively few develop ME.

If we want to talk multiple hits -- like a genetic immune disorder plus a common infection, or exercising heavily while you have a serious infection, then any of possibly hundreds of combinations could trigger ME. We really have little information to help us sort out what combinations could be problematic. Even then, how many people who exercise while ill (most professional athletes, for example) get ME? Almost none. We need combinations that explain why we got ME and others didn't. Exercise doesn't fit very well as a causal factor.

IMO, any supposed behavioral triggers are more likely to be patient-blaming (even if the patients is blaming him/herself) than any medical reality. We (and others) want to find a reason we got hit with this thing and other people didn't, so we look at what we were doing at the time -- working a lot, exercising a lot, not eating a perfect diet. But correlation is not causation. We need to look at what's going on in our bodies, not what we were doing at the time we first noticed symptoms if we want to track down causal elements.

I think it's useful to toss ideas around. Then we can check them out more carefully and formally. @Jonathan Edwards seems to think so (hope I'm not misrepresenting you, Prof!).

A poll would be a good idea, to see what kind of percentage of us fit this particular theory. There may have already been one - I know there have been some about onset and potential causes.

 

[MeSci]

Yes, but the main fear is that the infection could get worse etc. there is nothing to state that it could cause ME/CFS or any other disease.
It stands to reason that it might be harder to fight an infection if our bodies are stressed from exercise but why would that lead to ME / CFS ? That's the bit I don't follow.

OK - what's the reason we get PEM? We go into anaerobic ATP production too quickly - right? So the cause of ME - or the phenomenon that defines ME - is often thought to be this decline in our ability to produce ATP aerobically, is it not? What causes that? An auto-antibody to something in the chain of ATP production? @Jonathan Edwards has described clearly in detail how autoantibodies can be produced, including the randomness, but a possibility that an infection could increase the risk.

Obviously one will not realise that this has happened, so will continue to exert oneself as normal. Then one will crash = PEM.

The more we over-exert, the more we will crash, and the worse and more-prolonged the crashes will be. That's when ME will be more obvious, and worse.

Lipkin and Hornig have made potentially-useful discoveries about changes in cytokines over time in ME at the 3-year mark. But what causes these? And what do they cause?

Sorry - I have strayed from onset to progression!

 

[SOC]

Sorry - I have strayed from onset to progression!

Yes, but I think it's an important point. While the theory of exercise as a cause of ME has little to support it, exercise as a factor in progression is a different matter. My suspicion is that those who think of exercise as the trigger for ME may have simply experienced their first severe PEM episode after having ME for some period time at a milder level -- maybe days, or maybe years before the first severe PEM.

Truthfully, we know next to nothing about causal factors in ME and not much more about triggers (assuming the trigger concept even applies -- another unknown), so any number of theories are up in the air. Some fit the known facts better than others, so they currently look like better theories, but that doesn't make a certainty. It's still quite possible that some fundamental causal factors haven't even occurred to us yet.

We need more research. Now.

 

[Hip]

I would have thought that interferon was an unsuitable treatment for ME..

A significant side effect of interferon treatment can be depression, but if you battle through that, it can lead to excellent results in hepatitis C, fully eliminating the virus from the body in some patients, and thereby curing them.

Unfortunately in the case of enterovirus and ME/CFS, for some reason interferon does not seem to fully eliminate the virus from the body. If it did, then interferon would probably be a permanent cure for ME/CFS.

Dr Chia found that as patients got better on interferon, their enterovirus titers went down; and when they relapse, their enterovirus titers went back up again. So this provides evidence that enterovirus is playing a role in ME/CFS.



I know Dr Chia does not use interferon much now to treat ME/CFS, except in special cases. As far as I am aware, the reason is that he stopped using it is the great expense, the significant depression and other side effects, and the fact that after all the money and suffering, it does not lead to permanent remission from ME/CFS.

 

[MeSci]

Unfortunately in the case of enterovirus and ME/CFS, for some reason interferon does not seem to fully eliminate the virus from the body. If it did, then interferon would probably be a permanent cure for ME/CFS.

Only if/when the virus is involved in causation and/or perpetuation. This is not certain, and @Jonathan Edwards suggests that viruses may only be involved in a proportion of cases.

 

[Hip]

Only if/when the virus is involved in causation and/or perpetuation.

That goes without saying.

But since ME/CFS is often seen to appear immediately after viral infection, since enterovirus has been strongly associated with ME/CFS in numerous studies (not just in Dr Chia's), since ME/CFS symptoms often get better after interferon or oxymatrine treatments (along with a concomitant viral reduction in enteroviral load), and since when relapse occurs after discontinuation of these treatments, viral load is also seen to rise again along with the worsening of symptoms, there is a good argument for assuming enterovirus is involved in causation and perpetuation.

Oh and I forgot to mention that three separate brain autopsy studies all found an enterovirus infection in the brain of ME/CFS patients, but no such infection in healthy controls.

All good evidence to support the idea that enterovirus plays a causal role.



If we examine these remissions and improvements from an autoimmune angle, one might speculate that, as an alternative hypothesis, interferon and oxymatrine may be improving ME/CFS by ameliorating some underlying autoimmunity, rather than by reducing viral load.

However, from what I can gather, both interferon and oxymatrine have a tendency of triggering rather than ameliorating autoimmunity. For example, in hepatitis C patients receiving interferon treatment, 4% to 19% of these patients will go on to develop autoimmune conditions like lupus. Ref: 1

And Dr Chia himself has observed how oxymatrine can trigger rheumatoid arthritis in some ME/CFS patients.

So it seems unlikely that interferon and oxymatrine treat ME/CFS by reducing autoimmunity. Although if enterovirus were driving the autoimmune processes in ME/CFS, as some believe this virus does in type 1 diabetes, then the reduction in enteroviral load interferon and oxymatrine achieve in ME/CFS may indirectly lead to amelioration in autoimmunity.

It would be interesting to see if measurements of autoimmunity (such as autoantibody production) go down after interferon treatment in enterovirus-associated ME/CFS.

 

[BurnA]

Its funny how nearly every thread ends up with a discussion about whether this is a persistent viral infection or not.
We don't need to go over all those arguments here again do we?

 

[SOC]

Have you no respect? You forgot the 'Sir'. This man, clearly The Messiah for millions of sick people (or people who think that they are sick - poor fools), received a knighthood...

I recognize your sarcasm. Nevertheless, I feel compelled to rant about knighthoods and other given or purchased titles....

Since I don't buy into the whole titled superiour being thing, I don't feel the need to use titles of deference to refer to people. I'm happy to used earned titles, such as Doctor for a PhD, since I respect the hard work involved in earning that title. Knighthoods are not earned with hard work. They are political awards at best, and passed down through families with no effort to earn them at worst. As far as I'm concerned SW remains ordinary Mr Wesseley. In fact, I'm not even sure I want to give him that much respect. Simon seems good enough.

 

[SOC]

Its funny how nearly every thread ends up with a discussion about whether this is a persistent viral infection or not.
We don't need to go over all those arguments here again do we?

Yeah, it would be nice if this thread stayed on topic and didn't veer off into a discussion we've had a thousand times before. If people want to hash over the same old information, there's existing topical threads for that.

 

[Hip]

Its funny how nearly every thread ends up with a discussion about whether this is a persistent viral infection or not.
We don't need to go over all those arguments here again do we?

The arguments about whether or not ME/CFS is driven by a viral infection or some other pathophysiology is perhaps a tad off topic.

However, if we are discussing how exercise can precipitate an ME/CFS onset or relapse, then it is of interest how exercise might interact with the various pathophysiologies like viral infection or autoimmunity that are hypothesized to be behind ME/CFS.

In this earlier post, a speculated on a mechanism by which exercise might lead to a viral infection flare-up.

 

[BurnA]

Robin Soderling has had to retire from tennis - he believes training during glandular fever is a cause.

Robin Soderling: Swede retires from tennis after glandular fever - http://www.bbc.com/sport/tennis/35170939


Here is my take :

If the world no.4 tennis player continues to train and play with glandular fever then I think it's fair to say most sports people at some time in their lives have trained or played with some form of virus infection. Serena Williams played the semi final of the French open with the flu
Therefore if exertion with a virus was a big factor we should see more cases of cfs/me amongst sports people.

I think exertion whilst carrying an infection may be a factor but I believe most people who train /play sports with a virus dont get me/cfs therefore there must be a bigger factor at play.
Maybe it's the exact virus, maybe it's the exact time of exertion during the infection, most likely it's the immune response but how can we determine if exertion plays a role or not ?