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- At least eight studies have told us that when people with ME/CFS engage in a 2-day exercise test that their ability to produce energy drops the second day. While this appears to be one of the most anomalous findings in all of medicine all we know is that it applies to people with ME/CFS, in general.
- A Korean study asked if the same findings apply to people whose ME/CFS was triggered by a toxic exposure; i.e. would exercise one day produce the same drop in energy the next day?
- The study found that the toxin-injured ME/CFS patients switched from using the highly efficient and cleaner mode of aerobic energy production to the much more inefficient and dirtier mode of anaerobic energy production more quickly than the norm. It also appeared that their tissues were experiencing a reduced delivery of oxygen – the key component of aerobic energy production.
- The authors concluded that the results demonstrated “an underlying limitation in the exercise capacity to meet daily energy demands via aerobic energy production“. They also proposed that one of the chemicals in question that had damaged the mitochondria in smooth muscle cells, nerve tissues, and peripheral blood mononuclear cells was responsible for their reduced ability to exercise.
- That seemed to set the stage for a similar finding in a 2-day exercise study of people with another toxin triggered illness – Gulf War illness (GWI) but it was not to be. The 2-day exercise test found no drops in energy production or early entry into anaerobic energy production on the second day of the exercise test.
- Indeed, some earlier studies suggested that when it came to postexertional malaise, GWI might be very different from ME/CFS. One study found that about half GWI patients didn’t experience it. A more recent and comprehensive study found that while some people with GWI did experience increased symptoms after exercise, the group as a whole did not. Despite the other similarities between ME/CFS and GWI, PEM does not appear to play a significant role in GWI.
- Cooke has levied several critiques of the exercise studies in ME/CFS and has found that when he uses peak aerobic capacity as a starting point the findings indicating that energy production is disrupted in ME/CFS disappear. Instead, he believes that the problem in ME/CFS is reduced “aerobic fitness”.
- He proposes several hypotheses how this has happened the most prominent of which is that metabolic problems at the cellular level are impairing oxygen flows to the muscles – causing strange breathing patterns during exercise – and impairing ME/CFS patients fitness.
- While it may seem strange that two diseases, ME/CFS and GWI, that look so similar on the surface might be very different it should be noted that the ME/CFS community birthed the term postexertional malaise (PEM) because it was such a problem. PEM, however, has never figured in any of criteria for GWI.
- It’s possible then that because the Korean study studies toxin triggered people with ME/CFS that it naturally included participants who had both PEM and an inability to exercise. Since GWI does not produce significant amounts of PEM it stands to reason that people with GWI might not get as slammed by exercise.
- Small brain imaging GWI studies do suggest that exercise does have negative effects on the brains of GWI patients. The few joint GWI/ME/CFS studies done also indicate that while similarities exist differences do as well.
- These recent studies suggest that something other than problems with metabolism or energy production is producing GWI.
A recent Korean study, “A 2-day cardiopulmonary exercise test in chronic fatigue syndrome patients who were exposed to humidifier disinfectants“, asked how people with toxin-induced ME/CFS fared when subjected to the most intense test of all: the 2-day cardiopulmonary exercise test (CPET).
A Korean 2-day exercise test of toxin-induced ME/CFS essentially replicated past ME/CFS 2-day exercise study results.
The 2-day CPET test has been around for a long time but was little used until Staci Stevens and the crew at Workwell found it showed that exercise one day somehow inhibited the ability of ME/CFS patients to produce the same amount of energy during exercise the following day. This was a seriously anomalous finding, as past studies had shown that even people with serious illnesses were able to replicate their energy production over two days.
Since then, at least 8 ME/CFS studies have found that intense exercise one day damages the ability of people with ME/CFS to produce the same amount of energy the next day.
The Korean Study
The Koreans with ME/CFS had been exposed to chemicals put into humidifiers to prevent microbial overgrowth. While some people came down with lung damage, others without lung damage came down with an ME/CFS-like condition.
Instead of the bicycle usually used, a treadmill was used in 29 Korean patients who met the Fukuda criteria for ME/CFS. (While the Fukuda criteria are not the best criteria, the ME/CFS field did successfully use it for decades.) There was no healthy control group. Instead, the results of the first day’s test were simply compared to the second day’s test. If the results dropped more than expected (a 7% variation in results is allowed), an abnormal result was found.
The Korean 2-day exercise study found that intense exercise one day reduced the capacity to produce energy the next day.
The Koreans with chemically induced ME/CFS showed classic signs that other ME/CFS groups had shown on this protocol. The study found a reduction of 16.4% in energy production at anaerobic threshold (VO2@VT) – similar to that found in other ME/CFS studies (~26%,~16%,~22%). Plus the researchers found that the time to reach the anaerobic threshold was significantly reduced in the second test.
That suggests that the ME/CFS patients switched from using the highly efficient and cleaner mode of aerobic energy production to the much more inefficient and dirtier mode of anaerobic energy production more quickly than the norm. Using anaerobic energy production to power our bodies quickly results in fatigue. Plus, a decrease in the peak O2 pulse of 4.9% suggested that reduced delivery of oxygen – the key component of aerobic energy production – to the tissues in ME/CFS also occurred.
The authors reported that the results demonstrated “an underlying limitation in the exercise capacity to meet daily energy demands via aerobic energy production“. When it comes to producing energy, toxins, it appears, can trigger the same breakdown in energy production in ME/CFS as can infections. The authors proposed that one of the chemicals in question (polyhexamethylene guanidine phosphate (PHMG-p) had damaged the mitochondria in smooth muscle cells, nerve tissues, and peripheral blood mononuclear cells.
So far so good…
The Gulf War Illness Studies
Because nobody was probably exposed to more toxins in a shorter period of time than people with Gulf War Illness, one might expect the same results to show up in that group.
No such luck, according to Dane Cook and comrades. Cook has been digging into exercise and Gulf War Illness for about five years and during that time, some unexpected findings have shown up. His 2020 study, “Post-Exertional Malaise in Veterans with Gulf War Illness“, found that about half the GWI patients experienced post-exertional malaise (PEM) after an exercise trial while the other half didn’t.
Not only did Cook’s GWI studies find no reduction in energy production after exercise but no evidence of symptoms exacerbation in the group as a whole. (Image by Gerd Altman – Pixabay)
His 2021 study found an acute (one-time) exercise challenge did result in more muscle, fatigue and other symptoms and lower energy production in the GWI group, but those findings did not help explain who was to go on to experience post-exertional malaise. (One finding – which Cook did not use in that analysis – energy production at anaerobic threshold – did.)
Cook was a co-author of a third study led by Lindheimer, “An analysis of 2-day cardiopulmonary exercise testing to assess unexplained fatigue“, which did not find any significant drops in energy production or other CPET measures in the GWI patients from the first exercise test to the second (!).
Cook’s latest, more comprehensive post-exercise PEM GWI study also found no evidence that exercise impacted symptoms, pain sensitivity or cognitive performance; i.e. it did not produce PEM (!). The study reported that while some GWI patients did report increased symptoms (PEM) after exercise, the group as a whole (n=40) did not.
“Undesirable effects such as symptom exacerbation were observed for some participants, but the group-level risk of PEM following light-, moderate-, or vigorous-intensity exercise was no greater than seated rest. These findings challenge several prior views about PEM and lend support to a broader body of literature showing that the benefits of exercise outweigh the risks.”
The finding of that no PEM after exercise in GWI will surely trigger calls for graded exercise therapy, but a large cognitive behavioral therapy (CBT)/ exercise GWI clinical trial found that it produced only “modest” – and it was quite modest – help. Exercise is not going to return GWI patients to health.
My experience suggests that the Cook team could be right: exposure to toxins may produce chemical sensitivities and other problems, but they do not necessarily trigger PEM. In an effort to get rid of my chemical sensitivities, I participated in a sauna/exercise program at Dr. Rea’s Environmental Health Center in Dallas. I tried to engage fully in the exercise part of the program but had to quickly pull back. I was astonished to watch other chemically sensitive participants – many of them farmers and painters who had been injured by toxins – vigorously pedal away. They had no problems with exercise.
Kyle McNease’s story, on the other hand, demonstrates how exposure to toxins can produce an ME/CFS condition characterized by post-exertional malaise.
Cook’s Critiques
Cook has been trying to insert what he believes is more statistical rigor in ME/CFS exercise studies – rather unsuccessfully – since 2006, when he asserted that the findings needed to be matched for aerobic fitness (peak VO2 levels). Once that is done, he’s found that many of the problems with energy production disappear. People with ME/CFS fail on these tests, he believes, because they are less aerobically fit -not because they have problems with energy production, per se.
Far be it for me, a layman, to get into the middle of this but while peak VO2 is considered a valid measure of both aerobic capacity and endurance in healthy people one wonders if it’s necessarily so for ME/CFS? I have been told that peak VO2 – which assesses the highest level of energy produced during an exercise test – is among the least important measures of the CPET test for people with ME/CFS and that a more significant measure is how quickly they enter into anaerobic energy production. I know of a person with severe ME/CFS who has a very high peak VO2, who is still severely disabled, but can apparently at least temporarily generate high amounts of energy but who also enters almost immediately into anaerobic energy production.
Cook proposed that metabolic problems involved with oxygen extraction may be present in ME/CFS.
The question also remains, even if Cook is right, why people with ME/CFS would be “less fit”. Is it because they’re not getting much exercise – and if that’s the case – why is that? What is preventing them from getting more exercise?
While Cook’s approach discards several of the most significant findings from other CPET studies, Cook isn’t going psychological on us. In his big, multisite CDC exercise study, Cook proposed that the “unique” breathing issues he detected (which he also found in GWI) may reflect difficulty extracting oxygen from the muscles. He proposes that metabolic issues at the cellular level, and/or problems with red blood cell deformability, and/or a learned strategy to reduce symptom exacerbation or PEM could be in play. (Regarding the last hypothesis, one would have to ask why exercise is causing symptom exacerbation.)
Interestingly, the most anomalous finding in Cook’s study was a large increase in the “rate of perceived exertion” (RPE) in the people with ME/CFS. RPE tracks how effortful exercise seems to be. Cook believed the increase in effort in the ME/CFS patients might be caused by more effortful breathing patterns that attempt to wrench more oxygen out of the muscles. It also, interestingly, appears to fit with the Intramural Study findings suggesting that the brain attempts to slam the brakes on exertion by making it more effortful.
In Lindheimer et Al., Cook and colleagues also questioned whether the drops seen in the 2-day exercise studies are “clinically significant” because they lack “established reference values for absolute or percent changes”. They used a statistical method called smallest real difference (SRD) that adjusts for “standard error of the measure”, or measurement error, which can arise from a multitude of factors. (If I have it right – I’m poor at statistics – that assesses the variability of the sample results?)
Using that approach, they reported that a peak VO2 drop from 17.4% from day 1 to 2 for one veteran would not be considered to be “clinically significant”, and the person would not be considered to have PEM. (The person would have had to have a drop of over 22% for the drop of over a fifth in energy production to be considered “clinically significant”). I may very well be missing something, but I don’t get it.
Disability metrics have been developed specifically for CPET results, and two-day CPET results are used to demonstrate clinically meaningful reductions in the ability to work in disability cases. That doesn’t seem to be in question.
Conclusion
Not all fatigue, pain, sleep and cognition impairing diseases are the same.
The Korean and GWI study results seem contradictory. The Korean study seemed to extend the 2-day CPET findings to toxin-induced ME/CFS, while Cook’s study found no evidence of exercise-induced damage to energy production in people with an obvious toxin injury in Gulf War Illness.
This is despite the fact that, symptomatically, GWI looks exactly like ME/CFS. Note, though, that the criteria for ME/CFS and Gulf War Illness are different. The most accepted ME/CFS criteria require post-exertional malaise while the Kansas criteria for GWI – which was based on a survey of veterans – doesn’t mention it. (The Kansas Criteria mentions fatigue/ sleep problems, pain symptoms, neurologic/cognitive/mood symptoms, gastrointestinal symptoms, respiratory symptoms, and skin symptoms.) While the two groups are symptomatically quite similar, GWI appears to lack the signature symptom found in ME/CFS – post-exertional malaise.
That suggests the Korean study may have found reductions in energy production in its toxin-triggered ME/CFS patients because it used an ME/CFS criteria (albeit not a great one :)).
While the research focused on both diseases is limited, it does bear out the differences between the two. When Nancy Klimas looked under the hood of GWI and ME/CFS patients, she found both differences and similarities. Baraniuk has consistently found different brain signatures in the two diseases. Comparing the effect of exercise on ME/CFS and GWI patients, Baraniuk found opposite patterns of midbrain activation in them.
Exercise has been much less studied in GWI than in ME/CFS, where studies abound showing the negative effects of exercise. Small studies have, however, consistently found exercise is having an impact on people with GWI.
Baraniuk found that exercise triggered two different reactions – an autonomic reaction that was associated with brainstem atrophy in one group – and one associated with increased pain sensitivity and basal ganglia changes in another. Similarly, exercise improved working memory in one GWI group but impaired it in another. He also found altered cortical activity after exercise and deactivation of the default mode network after exercise in GWI, and exercise-induced postural orthostatic tachycardia syndrome (POTS) in a subset of people with GWI.
Cook’s study suggests that the post-exertional malaise symptom is crucial part of ME/CFS but not of GWI. In a way, that’s a not a surprise – the post-exertional malaise term was, was after all, birthed by the ME/CFS community because it was an obvious manifestation of the disease that was not being taken into account. Problems with “fitness”, metabolism, aerobic energy production – whatever term you want to use – all follow on from that.
Cook’s findings suggest that problems with metabolism or energy production are not present in GWI which lacks PEM; in other words, there’s more than one way to produce a disease with symptoms like fatigue, pain, gut, sleep and cognitive issues.
I think ME/CFS is not the same disease as GWI. Making a comparison between a double exercise test of these 2 different diseases on the basis of toxins – which toxins? – can lead to wrong conclusions. In ME/CFS it can also be bacteria that produce toxins. Condition in ME/CFS plays a role, but is absolutely not the cause of the major differences between the 2-day exercise test. Even after 48 hours, large differences are found between the 1st and 2nd CPET test.
https://pubmed.ncbi.nlm.nih.gov/33947430/
However this is interesting: ”Cook proposed that the “unique” breathing issues he detected (which he also found in GWI) may reflect difficulty extracting oxygen from the muscles. He proposes that metabolic issues at the cellular level, and/or problems with red blood cell deformability,…. ”
Our organization collects data on all kinds of birth defects and exposures of the fathers and mothers. We have two special sections for military exposures, one for exposures in Vietnam and the other for exposures in the first Gulf War.
In 1995, we identified an unusual increase in a rare cranial-birth defect in the children of Gulf War veterans and I was invited to present our data to the Presidential Advisory Committee on Gulf War illnesses in 1996.
Gulf War veterans had been potentially exposed to 31 categories of reproductive toxicants. These are toxic exposures that have caused birth defects in either animal and/or human studies.
The Department of Defense funded a study of the birth defect we had found increased and discovered a tripling of this defect in Gulf War veterans’ children who were born in military hospitals. They did have not access to additional cases born in civilian hospitals that we had. If they had these cases, their study would have reached statistical significance.
What does this have to do with this recent article? Toxins that are reproductive toxicants can also cause deleterious effects in the exposed adult. It is impossible to determine all of the exposures or their combinations different veterans had out of the 31 possibilities. But, exposures to all toxins don’t result in the same outcome.
The study authors are proceeding as if all cases of Gulf War Syndrome are the same. They are not.
In evaluating any study, you must always look at the raw data, not the statistical outcome. If there are questions about the raw data, the outcome is questionable.
I agree with you 100%. In 1994-1995, I participated in the GW protocol in WRAMC but did not have this data until 2016. All labs were completed by Infectious Disease Human Subjects at WRAIR (previously employment) but each of us prior to deployment had different exposure experiences before deployment and during deployment which is extremely important but also complicated. I had a fellow veteran that had children with birth defects as you stated. The data was there but we just didn’t know it as veterans at the time. Thank you for your work.
https://www.theguardian.com/environment/2001/jul/30/internationalnews
☝️most of these soldiers were given at the very least ten vaccines.
I’ve always been of the belief,and moreover now than ever, that my childhood vaccines did this to me.
One of the most toxic elements known to mankind (ETHYL MERCURY)
was injected into millions of us. ALL FORMS OF MERCURY IS TOXIC
my early school years were a blurr…I failed gr
7 and 9 and dropped out after. I held several jobs until all hell broke loose in 1993. I had no idea a human could become this sick.
I swear this is a big cover up…and already we are seeing big pharma drugs entering into this.
The fact that nothing causative being found is disturbing to me.
My next door neighbor is in the army and is involved in a class action law suit for vaccines being given…not sure if it was gulf war illness
The chemical over exposure that tipped me over the edge was a harmless hardwood floor finish that any normal human being could have tolerated.nothing toxic about it….water based
I believe childhood vaccinations did me in as well. We also lived by an airport in Seattle so possibly exhaust from planes & cars back in the 1960s was too much for my system.
Not to mention, if we were born in the era of leaded gasoline.
I’ve tested pos. For uranium, nickel and antimony….lead was also tested but came up zero which to me is impossible given the fact that my dad was a stock car racer, my uncle a very famous double AA fuel dragster racer.
My brother and I were right in there working in all that leaded fuel from a very young age.
Like I stated earlier, why havnt the researchers been able to find these accumulations.
Heck, I recall a lady won a law suit over cancer causing tampons and the scientist was able to find it
Right? I remember driving on the freeway & getting sick from the gas fumes.
We’re a sick society that needs better air quality & food regulations.
As a child growing up in the 60s & 70s, there were no cancer centers.
Now, they’re all over the place.
It’s sketchy & scary.
A co-worker’s husband had stage 4 (incurable) cancer.
They went to Mexico for treatment. He came back cancer free.
Something is fishy here in the U.S. 🙂
Let’s see….hmmm…what could cause a person’s cells to have zero electricity between each cell….maybe a foreign metal that is a great conductor…lead or mercury
And…just to add…I’ve read for years that heavy metals end up at the base of people’s brains
They continue to use lead in aviation fuel in the smaller non commercial planes
Why was prof. Garth Nicholson’s office and lab raided by the US army when he was working to find out what gulf war illness is?
Hugely understudied are the Iraqi soldiers from the other side 🚩
Yes, and I was going to say what about the civilians too.
For me this raises the question of how many people diagnosed with ME/CFS actually have something that would more accurately be defined under GWI (despite never having been in the Gulf War). Because since I’ve connected with many other ‘pwME’ it’s become clear that while they are just as sick and experience similar symptoms, some do not have as clear a relationship between physical activity and PEM as others. Their symptoms seem to arise spontaneously or are chronically present, whereas mine very clearly fluctuate in direct response to physical activity/stress. The inverse of this observation is that, for me, rest eventually and reliably results in floating back up to baseline, while for others rest seems not to result in an improvement. I would almost rather have my version, which I call ‘Classic ME’ because I can be reasonably confident that aggressive rest will inevitably bring relief. but the problem of course is that we are all artificially grouped together in one homogenous medical diagnosis.
Geoff, I couldn’t agree with you more. I am much like you and require a period of complete rest to ‘drift back’ to a moderate (albeit low) energy level. I also can become energy depleted with non-physical activity/stress. I notice a common energy pattern in myself–after the pain meds kick in, If not depleted, I have a moderate amount of energy for about 4 or 5 hours but the energy drops after that–sometimes to nothing. I get a small circadian bounce late night–and rinse and repeat. I do often just feel crappy generally and right now I have had a sore throat, headache and general malaise for several weeks. I don’t call it a ‘crash’ but something isn’t working right. Then add more than a sprinkling of Ehlers-Danlos.
There are so many different factors and therefore versions of this, I do agree it is not helpful to lump them all together.
I’ve always thought GWI was most similar to fibromyalgia rather than CFS.
I don’t have the spoons rn to read this as thoroughly as I want to but afaict there’s no mention of gender, which strikes me as odd… iirc about 95% of gulf war military personnel were male, whereas about 75% of people with ME are female. I would have thought this is a crucial factor to consider wrt any distinctions between the two diseases, and an important differentiator to investigate when reviewing the findings of any relevant studies.
According to this study, 23 veterans who had been diagnosed with Gulf War Illness showed an abnormal drop in cerebral blood flow velocity upon executing a “sit to stand” test.
The authors appear to prefer this quick movement to the slightly slower movement of a tilt table, although they don’t seem to say why. Perhaps they wanted to measure what would be happening in everyday life.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0205393
I wonder whether they would have also found low blood volume if they could have tested it.
Twenty out of 23 were male in the study I linked to.
Good point given the gender divide we’ve seen in ME/CFS :). Most of the soldiers were men but the gender difference between ME/CFS and GWI really complicates things.
How about that – a pretty important commonality. Reduced blood flows to the brain are surely a major deal in ME/CFS and now GWI. The plot continues to thicken! :). I don’t know why we don’t have more blood volume studies in these diseases…
Yes, if any scientists are reading this, there is a simple way to measure blood volume available now, no need for isotopes. It’s used by NASA to investigate loss of blood volume in astronauts.
https://detalo-health.com/
There’s a scientific version, validated for research only, and a medi al version, which can be used for research and clinical applications.
The medical version was approved in the EU in 2023. Just need someone in another country to take the (small) leap to purchase one.
Pem can develop from physical exercise , as done here, or from s mental test. So, what about subjecting GWI patients to a mental test? Do they develop pem in those cases (and stating that the cpet test is only useful for people with a muscle fatigue)?
Good question particularly given the brain findings in GWI. My Oura ring finds that mental work is often more stressful than physical work.
Beste Cort ,
Dankjewel voor al je inspanningen, maar ik heb de laatste tijd het gevoel dat er teveel andere aandoeningen bij worden gehaald met erg veel aannames.
Ik zie iig door de bomen het “ ME” bos niet meer.
Vriendelijke groet
Google translate
The forest does seem to be getting denser doesn’t it – and you’re right – we all thought that people with GWI would have the same results on the exercise test. (It is interesting that they have similar breathing patterns as people with ME/CFS). It looks like there will be commonalities and differences – and that what we really need are more studies that carefully compare these conditions. We don’t even have many ME/CFS / fibromyalgia studies.
Hi Cort….with regards to the lack of PEM in some GWI participants …it doesn’t surprise me. As with everything there are degrees of symptoms based on things like amount of exposure, underlying health , genetics, ability to naturally detox , age , sex etc.which in turn govern the amount of damage . I have classic/ severe CFS symptoms and PEM from a drug . Not everyone gets harmed from this drug and even people who are severely harmed recover in time while others never do or continue to worsen. Also there’s a huge diversity of symptoms reported. Some report CFS systems but simultaneously describe how wonderful they feel after a gym workout …… hmmmmmmm Anyway maybe I’m overly simplistic but it’s back to square one….the cellular level and mitochondrial function disorder. Many toxins ( mercury, lead etc) interfere with either the production of energy on block ATP from reaching its target . ” Or…. Maybe I totally missed the point in that I could hardly get through the gist !!!! Oh I hope someday we can pour all these diverse studies/ results into AI ….wouldn’t that be something ?!?!
Thanks for your unrelenting efforts to keep us informed 🙏🏻🙏🏻🙏🏻!!
I’m a veteran and suffer from GWI. This article confirms my own research in exercising with GWI. Although I’m able to exercise at a moderate to high rate at times my ability to breathe and utilize the oxygen uptake is extremely difficult. I experience PEM but not always, in addition, other conditions of which hinder my pulmonary functioning are restrictive lung function, iron-deficieny anemia, LC-MGUS, asthma, hypo-inflation and inability to utilize oxygen properly and expel CO2 is a huge challenge leading to extreme fatigue.
As I continue to search for answers to better my health, lower risks factors, and find treatment methods both medicinally and naturally it is still extremely frustrating process. The VA NIH and other organizations don’t necessarily trickle this new information to the practitioner level. As I’ve explained for several years to both private and VA doctors, “I can’t breathe or get enough oxygen”, isn’t taken as seriously as it should.
Thank you for this article it will help me in the future as I blindly navigate GWI and my health moving forward.
Thanks so much for giving us insights into your GWI, Cori. Interesting that low CO2 are showing up in all these diseases! A recent fibromyalgia study found it in about 40% of patients.
One nice note for GWI – there are, I believe, a good number of clinical trials underway.
Good luck with everything and thanks again for sharing your experience 🙂
Hi Cort,
Thank you for the support. Actually, my CO2 levels are high not low.
My lungs do not expel the outgoing CO2 sufficiently leading buildup in my body and low oxygen saturation levels, but knew what you meant. 😊 It’s still problematic nevertheless.
Got it – I change it to CO2 problems 🙂
Hi Cori, and THIS!! I e told docs for decades, VA and cov, that I can’t breathe deeply enough to get enough O2!! I participate in allllll the research studies, and have been to WRIISC, and plan on going back! But have gotten zero traction with my pact team… I really don’t want to even make appointments, k owing they blow me off.
Hi Michael,
Thanks for your comment. If I may offer a few suggestions without getting into specifics about your situation, first – change primary care doctor if unhelpful (there is a form to complete). Two – reach out to the patient advocate office via the VA.gov site to file a complaint. Three – if all else fails reach out to the hospital Chief of Staff and explain your situation. I’m sorry you’ve had troubles and it’s unfortunate but a sad reality. I hope that one of these actions will help you get on the track toward better care and health.
The blog is partly talking about how GWI and ME/CFS may be different because not all people with GWI have abnormal 2-day CPET:
“Indeed, some earlier studies suggested that when it came to postexertional malaise, GWI might be very different from ME/CFS”
But this seems like the same thing as long COVID vs. ME. After some inciting event (sarin gas/pesticides or SARS-CoV-2 exposure) many people develop long term symptoms, but not everyone has the symptom of exercise intolerance.
It’s a weird comparison, like comparing “complications after falling off a cliff” and “brain damage” and saying these two are not the same thing because not all people who fell off a cliff have brain damage but all people who have brain damage do have brain damage.
A better comparison would be, how different are GWI and long COVID.
” His 2020 study, “Post-Exertional Malaise in Veterans with Gulf War Illness“, found that about half the GWI patients experienced post-exertional malaise (PEM) after an exercise trial while the other half didn’t.
Cook’s latest, more comprehensive post-exercise PEM GWI study also found no evidence that exercise impacted symptoms, pain sensitivity or cognitive performance; i.e. it did not produce PEM (!). The study reported that while some GWI patients did report increased symptoms (PEM) after exercise, the group as a whole (n=40) did not.
‘Undesirable effects such as symptom exacerbation were observed for some participants, but the group-level risk of PEM following light-, moderate-, or vigorous-intensity exercise was no greater than seated rest. These findings challenge several prior views about PEM and lend support to a broader body of literature showing that the benefits of exercise outweigh the risks.’
The finding of that no PEM after exercise in GWI will surely trigger calls for graded exercise therapy, but a large cognitive behavioral therapy (CBT)/ exercise GWI clinical trial found that it produced only “modest” – and it was quite modest – help.”
It’s strange to say “while some GWI patients did report increased symptoms (PEM)” and then a couple sentences later “The finding of that no PEM after exercise in GWI”.
“The Korean study seemed to extend the 2-day CPET findings to toxin-induced ME/CFS, while Cook’s study found no evidence of exercise-induced damage to energy production in people with an obvious toxin injury in Gulf War Illness.
This is despite the fact that, symptomatically, GWI looks exactly like ME/CFS.”
This all is odd. Even if the Korean study used people that got ME after humidifier disinfectant exposure, which it’s unclear they did, presumably it wasn’t every person who got symptoms after HD exposure that got ME. Likewise Cook’s study found evidence of PEM in some people with GWI, not “no evidence”.
And the last sentence (“symptomatically, GWI looks exactly like ME/CFS”) doesn’t even make sense if claiming one group has PEM and the other doesn’t.
I fear people will take this blog to mean all people with GWI can or should exercise.
I think there’s an obvious error here. The aim during exercise is to extract oxygen from the air and transport it to the working muscles, not to extract oxygen from the muscles!