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End game?

Messages
85
I have come to terms with CFS/Gulf War Illness as my reality for the past 25 years, but I as I age the cycles become far worse to the point that there is no discernable cycle just bad days and worse days. Other veterans (the only other CFS folks I know personally) are finding the same thing to be true. The oldest of us are in our sixties and the youngest are perhaps 30 or so and have returned from combat in the desert fairly recently.

So naturally I am starting to wonder what the end game is? If anyone has insight into how CFS progresses as we reach our "golden years"? My guess is that at 61 now I can expect the fatigue, memory issues, POTS and the rest will accelerate and become terminal at some point. Not trying to be Debbie Downer but in lue of much greater understanding much less a cure I feel I need to face what seems inevitable.

On a financial planning note, has anyone seen a situation where CFS is deemed the cause of death? The reason I ask is that many of us veterans are entitled to full benefits when diagnosed with Gulf War Illness related conditions. Those benefits only continue for the spouse if death is caused by service related conditions.

Thanks!
 

percyval577

nucleus caudatus et al
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1,302
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Ik waak up
I knew a man for a short time who then was 75 years of age (interestingly a Prof for Psychology). His illness sat on quit late with EBV, he was almost 50 if I am remembering right.
He said it would get worse and worse. He was able to laugh but must have felt bad. I was new then and indeed bad as well. We both could move around and do something. He still did some work, but it might be that he had lessened to work earlier when he was regularly employed, I cannot remember. For me it was obvious that he those days got more worse than before.

I havn´t read much about the gulf war illness and cannot judge how it could be caused (explosions, wasn´t a guess like so?). To this man though, I would say now, don´t eat pulse, you will get worse by it.


PS: I remember now, he turned 80 only a few years later when he was about to stop or just had stopped his seminar(s). I have corrected the age to 75.
 
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Sushi

Moderation Resource Albuquerque
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19,935
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Albuquerque
On a financial planning note, has anyone seen a situation where CFS is deemed the cause of death?
I know of a very few cases where the death certificate said CFS--but this is extremely rare.

As for things just getting worse and worse in later years, I think that there are a few things to consider: we don't know for sure the likenesses and differences between Gulf War Illness and ME/CFS but we have many members here who are in their 60's, 70's and a few in their 80's. And while each of us has an individual experience, I'd don't recall that most people report a marked worsening of symptoms as they age.
 
Messages
85
I havn´t read much about the gulf war illness and cannot judge how it could be caused (explosions, wasn´t a guess like so?). To this man though, I would say now, don´t eat pulse, you will get worse by it.

GWI or GWS as it was called is probably caused by multiple concurrent exposures to a variety of toxins and chemicals but as with CFS as stand alone condition...who knows. The primary conditions mirror CFS but with rashes, nasty autoimmune symptoms etc. At least now it recognised as a real syndrome, and it was first described and studied in 1994. Most of us (200K worldwide) were deployed between 1990 and 1992 when we became sick. Mostly after GI viruses.

We really need to combine the research efforts and knowledge as people like Dr Klimas has.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
You could expect that age related health decline and CFS/ME/GWI deficits would have a cumulative impact.

So far as I am aware there is no specific epidemiology for ageing patients with ME or CFS. There is a dearth of good epidemiology in its entirety, though I do not closely follow GWI research.

It is not clear that CFS and ME and GWI have the same patient cohort, it seems they are related cohorts but not identical.

I am 57 and have been slowly getting worse for five years, but the last six months have shown a slow improvement. Its very hard to be sure about what to expect, the science does not really exist. So in planning it would probably be a good idea to be conservative about guesstimates.
 
Messages
85
There are probably more studies into GWI than stand alone CFS in truth. Researchers are now finding certain biomarkers to do with inflammation from autoimmune conditions linked to both CFS and GWI. I know the VA has funded several metabolomic studies concerning GWI, and the "experts" on GWI do believe mitochondrial dysfunction is a big contributor.

https://www.sciencedirect.com/science/article/pii/S0300483X16302566

Looking at your posts they remind of another similarity, dismissing CFS and GWI as a psychosomatic condition. In veteran cases it was blamed on PTSD.

There are several studies that link CFS with GWI. And some that claim they are distinct diseases. Until we know what causes each and why the symptoms often mirror each other it would only make sense to combine the efforts. There seems to be a reluctance in the CFS community to do so, which I find rather odd given funding by the Department of Defence and VA dwarfs that of other sources of funding. No logical reason to slam doors shut on ourselves.

https://www.ncbi.nlm.nih.gov/pubmed/15941694
 
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wigglethemouse

Senior Member
Messages
776
Have you seen all these clinical trials Nancy Klimas is running on GWI? GWI has $40MM funding in US.
Klimas Clinical Trials

Her presentations state that GWI has hypermetabolism vs ME which has hypometabolism. Also Congress/DoD has a mechanism to fund trials for GWI but not ME. She has cured GWI in a GWI mouse model and is now trying the same thing in both GWI and ME.

So hang in there @Desertstorm
 

percyval577

nucleus caudatus et al
Messages
1,302
Location
Ik waak up
GWI or GWS as it was called is probably caused by multiple concurrent exposures to a variety of toxins and chemicals but as with CFS as stand alone condition...who knows. The primary conditions mirror CFS but with rashes, nasty autoimmune symptoms etc. At least now it recognised as a real syndrome, and it was first described and studied in 1994. Most of us (200K worldwide) were deployed between 1990 and 1992 when we became sick. Mostly after GI viruses.
We really need to combine the research efforts and knowledge as people like Dr Klimas has.

There is also Lady Margret who has got ill (immediatly I think) when dealing with sheep dip.

Ever my first guess is it would be all the same under different circumstances. It feels like so, but it is also a generel method: to start with the most bold and then try to hold it.

In my opinion it´s nitric oxide depending on manganese levels averaged over time and strength of stressors. I though wondered with the explosiontheory, but it might be a possible cause nevertheless.
 
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FMMM1

Senior Member
Messages
513
There are probably more studies into GWI than stand alone CFS in truth. Researchers are now finding certain biomarkers to do with inflammation from autoimmune conditions linked to both CFS and GWI. I know the VA has funded several metabolomic studies concerning GWI, and the "experts" on GWI do believe mitochondrial dysfunction is a big contributor.

https://www.sciencedirect.com/science/article/pii/S0300483X16302566

Looking at your posts they remind of another similarity, dismissing CFS and GWI as a psychosomatic condition. In veteran cases it was blamed on PTSD.

There are several studies that link CFS with GWI. And some that claim they are distinct diseases. Until we know what causes each and why the symptoms often mirror each other it would only make sense to combine the efforts. There seems to be a reluctance in the CFS community to do so, which I find rather odd given funding by the Department of Defence and VA dwarfs that of other sources of funding. No logical reason to slam doors shut on ourselves.

https://www.ncbi.nlm.nih.gov/pubmed/15941694

This is from the link you posted [https://www.ncbi.nlm.nih.gov/pubmed/15941694]: "chronic fatigue syndrome (deployed, 1.6%; nondeployed 0.1%; odds ratio, 40.6 [CI, 10.2 to 161])". An odds ratio of 40 means that chronic fatigue syndrome is 40 times more likely to be present in the deployed group than the controls.

Others have pointed out that James Baraniuk's studies on Gulf War Veterans included people with ME/CFS as controls; thereby, he contributed significantly to ME/CFS research [proteomics]. He's recently published a paper (2017) on leaky blood/brain barrier; from memory this looked at Gulf War Veterans and included people with ME/CFS.

Nancy Klimas has done a bunch of publicly funded research on Gulf War Veterans which reads directly across to ME/CFS [e.g. title - "Using gene expression signatures to identify novel treatment strategies in gulf war illness"].

Others have pointed out that you couldn't get funding for ME/CFS research so the use of people with ME/CFS as controls, in studies on Gulf War Veterans, produced some of the significant ME/CFS studies.

Couldn't agree more i.e. that we don't know what causes each disease --- some claim they are distinct diseases. Ron Davis recently said that the symptoms in ME/CFS could be genetic [https://www.omf.ngo/2018/05/01/dr-ron-davis-wbur-video/].

To me the recent publication regarding Epstein-Barr virus [title - "Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity"] supports the view that environmental stressors can increase the risk of (immune) disease. From memory Baraniuk highlighted the exposure of Gulf War Veterans to anti nerve agents, pesticides ----; maybe that was their environmental trigger. Maybe for some people with ME/CFS the environmental stressor is Epstein-Barr virus.

I'm not aware of any resistance in the ME/CFS community to working with Gulf War Veterans. As well as better access to funding for studies on Gulf War Veterans, the odds ratio of 40 means that cooperation makes sense.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Until we know what causes each and why the symptoms often mirror each other it would only make sense to combine the efforts.
This only works if the studies are stratified, or if its a direct comparison on various measures into particular diagnostic definitions of GWI and ME or CFS. Otherwise it creates a hash of scientific analysis. Let me give you a worst case scenario. Suppose they discover a potential cure for GWI. They do a study on a GWI+CFS cohort and it does not work. Then years later, maybe after data reanalysis, they discover it worked for GWI but not for CFS. For cure you can also substitute treatment or biomarker. This kind of cohort combination also increases the cost and difficulty of analysis.
 
Messages
85
This only works if the studies are stratified, or if its a direct comparison on various measures into particular diagnostic definitions of GWI and ME or CFS. Otherwise it creates a hash of scientific analysis. Let me give you a worst case scenario. Suppose they discover a potential cure for GWI. They do a study on a GWI+CFS cohort and it does not work. Then years later, maybe after data reanalysis, they discover it worked for GWI but not for CFS. For cure you can also substitute treatment or biomarker. This kind of cohort combination also increases the cost and difficulty of analysis.

I never have been one to accept "what ifs" as an excuse for inaction. Unless I am way off base the Klimas studies do make direct comparisons.

CFS as DX'd within the GWI parameters is still CFS. It does not seem reasonable to have a condition that exactly mirrors itself right down to IBS, POTS, onset after a virus etc and not compare them or study them as the same condition. It is as if we have measles and another seemingly identical condition being called, say, "wongertate" and not at least try to find common causes and treatments.

Cheers.
 

FMMM1

Senior Member
Messages
513
This only works if the studies are stratified, or if its a direct comparison on various measures into particular diagnostic definitions of GWI and ME or CFS. Otherwise it creates a hash of scientific analysis. Let me give you a worst case scenario. Suppose they discover a potential cure for GWI. They do a study on a GWI+CFS cohort and it does not work. Then years later, maybe after data reanalysis, they discover it worked for GWI but not for CFS. For cure you can also substitute treatment or biomarker. This kind of cohort combination also increases the cost and difficulty of analysis.

Possibly you could stratify based on sphingolipids or the altered cell respiration (can't remember name of apparatus). It seems like a chicken and egg scenario; when you have the biomarker you understand the underlying problem but in order to identify the biomarker you need to understand the underlying problem.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Possibly you could stratify based on
In an investigative study they usually use some kind of cluster analysis.

It is the current case that we do have biomarkers. Lots of them. We just don't know if they are diagnostic. So analysis based on those can proceed right now, though with the caveat that some markers will later be shown to be not important.

In any cohort that is hypermetabolic, it is very unlikely, based on current science, that they have the same problem as in ME.

I think it likely that CFS will fracture into many diseases. Its one of the reason I do not like CFS diagnoses, and prefer the more modern ME definitions ... they are not guaranteed to be accurate but the odds are much better. ME in turn may well be several diseases, although it might be a spectrum, or one disease with several to many manifestations.

Here is the big caveat. Some diseases have multiple forms, or manifestations. Given the complexity and body systems involved in ME it might be one disease with many symptom variations. One critical thing I think should be kept in mind by researchers is there might be one to many molecular switches. If the disease is switched one way, you get different symptoms to it being switched another way. Leishmania is a disease, in which the immune state determines the course of the illness, but I am sure there are others.

So the fact is we do not know the relationship between GWI and CFS and ME in enough detail to be sure of much. For this reason the different cohorts need to be considered separately, though these can all be in one study. It might be, for example, that a subgroup of GWI and a subgroup of ME are the same. This is worth finding out. It however is unlikely to be discovered if we do not design studies to at least have a chance to show such issues.

GWI and ME and CFS diagnostic criteria create different cohorts. This necessarily means some kind of selection biases might be in play, and so have to be accounted for. Any identifiable potential bias needs to be considered in developing a study methodology.

The hallmark feature of ME is PEM, not fatigue. PEM can be demonstrated using the two day CPET and now various blood measures. If GWI patients show that, then they either have ME, or both ME and GWI, according to current understanding. It would not surprise me if one to several percent of GWI patients also have ME, just as I think it possible to have HIV or AIDS and ME even if diagnosis is problematic.

When looking for biomarkers, especially diagnostic biomarkers, its very important to keep a cohort as strictly defined as you can. Later, when we have diagnostic biomarkers, you can consider overlapping cohorts. If you merge cohorts, and don't stratify the data, biomarker discovery will be very problematic. For this reason Ron Davis is focusing on very severe patients, not even typical patients. This will increase the strength of the signal we are looking for, at least for some signals. This makes discovery easier.

Let me give a related example, and one that applies to me. It was discovered there is a subset within ME with a stable cytokine signature. That subset is encephalitis survivors. We do not yet know if this is the same as ME, but its very likely that many encephalitis survivors have diagnosed or undiagnosed ME. Further research needs to take this into account, and stratify the analysis accordingly. We cannot just presume they are the same disease until we understand what is going on. Do encephalistis survivors show a typical two day CPET result, for example? I don't know.

Big advances in medicine usually come from splitting cohorts, not lumping them together. You can only lump things together, and get good results, if the likely differences in subgroups will not confound the outcomes being measured. Sometimes you will not know if they will or they will not until long after the study is done.
 
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Messages
85
In an investigative study they usually use some kind of cluster analysis.

It is the current case that we do have biomarkers. Lots of them. We just don't know if they are diagnostic. So analysis based on those can proceed right now, though with the caveat that some markers will later be shown to be not important.

In any cohort that is hypermetabolic, it is very unlikely, based on current science, that they have the same problem.\ as in ME.

I think it likely that CFS will fracture into many diseases. Its one of the reason I do not like CFS diagnoses, and prefer the more modern ME definitions ... they are not guaranteed to be accurate but the odds are much better. ME in turn may well be several diseases, although it might be a spectrum, or one disease with several to many manifestations.

Looking at the "symptoms" forums listed on the homepage here, they ALL coincide exactly with symptoms of GWI. That could not be a coincidence in my mind. How studies are carried out is not my speciality and far beyond my scope, but given it is established that GWI does result in CFS in most who were exposed in the desert or did contract viruses I think studying any links or similarities between them could only advance our knowledge of both conditions.

In my experience with CFS and GWI umbrella it needs to be looked at by a multitude of specialists given there is such a wide variance in symptoms, but fatigue being the most debilitating result . I have gone to two multi specialty screenings at Mayo and one at Stanford via Palo Alto VA. All three were useless because no two docs were ever on the same page and some even refused to acknowledge the condition citing data from 20 years ago. Another reason in my mind to get some cohesion into the research...which requires funding. And such funding is far more apt to be granted through the VA and DOD than CDC etc sadly.

I read where one group is proposing to combine ME/CFS and some of the GWI symptoms under SEID. Anything to change the perceptions of the ignorant will help also.
 
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pattismith

Senior Member
Messages
3,932
Did you try an association between T3 + prednisolone?

I got worse and worse for 35 years, and I am fine since I started this.
Low T3 state/syndrome worsens with aging, so if you have thyroid resistance, or central hypothyroidism, aging will have a negative impact.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
I read where one group is proposing to combine ME/CFS and some of the GWI symptoms under SEID. Anything to change the perceptions of the ignorant will help also.
Science struggles with dealing with things based upon symptoms. Similar symptoms means patients can understand what other patients are going through, but its been a disaster for science.

Take type 2 diabetes ... a century of research and they are still struggling to figure out what it is. I realised some years back that its a syndrome, a cluster of symptoms and findings. Now they are finally splitting it into five different diseases, or at least subtypes.

Cancer went the same way. Modern progress is mostly about splitting a cohort, with similar symptoms, based on molecular pathology. That pathology is what is important, symptoms are just clues. Symptoms sometimes confuse the science.

Depression is another case in point. While its often a debilitating and even dangerous symptom, its just that ... a symptom, or more accurately a range of similar symptoms. When underlying causes in some subsets have been treated, with vitamins or antivirals for example, it goes away. Antidepressants are a lot like handing out aspirin to treat a headache, whether or not its due to vascular issues, migraine, brain tumour or impending stroke.

Fatigue is the single most common symptom. Its not very important to focus on it because it tells you very little by itself. Its also typically not disabling. Its the other things that are associated with fatigue that are disabling, and confusion over terminology and explaining things has a big part to play in this. What is worse, chronic fatigue is not, despite claims, universally present in ME patients. Fatigability, and symptom exacerbation from activity, are more central to the issue. Its not exercise intolerance either, though I think we have that too. Its about the underlying pathology getting worse after activity, in what patients describe as a bad crash, or PEM. We are finally figuring out tests to measure this. Biomarkers can change our understanding profoundly.