By David Tuller, DrPH
I haven’t had time to cover the new and wildly over-hyped study about prolonged fatigue–and purportedly about “chronic fatigue syndrome”–that was published this week in the journal Psychoneuroendocrinology. Thanks no doubt to the involvement of the Science Media Centre, this mildly interesting piece of research has received widespread media attention.
Since the study team included confirmed members of the biopsychosocial ideological brigades, I remain wary of the motives of those involved. Even more so since this group of researchers apparently continues to define the illness using the discredited Oxford criteria, as they do in the Psychoneuroendocrinology study. This case definition requires only six months of unexplained fatigue and is known to generate heterogeneous populations of people suffering from a range of fatiguing disorders.
Given these findings, will biopsychosocial researchers soon be promoting GET and CBT as appropriate therapies for the reported immune dysfunction? Or are they so worried that the field is moving beyond their discredited “deconditioning/unhelpful beliefs” model that they’re desperate to stake a claim on some biomedical aspect?
This paper documents that a particular form of immune activation can lead to a prolonged state of fatigue, even after the stimulus has ended. It is unwarranted for the authors, the SMC or anyone else to make anything other than extremely speculative and cautious claims at this point about any relevance of these findings to ME/CFS. Instead, in presenting the results, they have dramatically overstated the case–and, as usual, the media herd has followed their lead.
Here’s a handy overview of the study from MEAction:
And here’s an insightful post from Nick Brown, a psychology graduate student at the University of Groningen in the Netherlands. Brown was profiled earlier this year in Science magazine as one of the “data thugs” taking down poor-quality research through reanalyzing results.
I’m posting Nick’s blog in full below, with his permission.
Have scientists found an explanation for the onset of ME/CFS?
In this post I’m going to discuss this article (the link leads to a page from which you can download the PDF; I’m not sure if this will last), which appeared today (17 December 2018):
Russell, A., Hepgula, N., Nikkheslat, N., Borsini, A., Zajkowska, Z., Moll, N., . . . Pariante, C. M. (2018). Persistent fatigue induced by interferon-alpha: A novel, inflammation-based, proxy model of chronic fatigue syndrome. Psychoneuroendocrinology. Advance online publication. http://dx.doi.org/10.1016/j.psyneuen.2018.11.032
(Notes for nerds: (1) The article date will become 2019 when it appears in print; (2) There are 20 named authors, so I’m glad that APA referencing style only requires me to list the first six and the last one. I will be calling it “the article” or “the study” or “Russell et al.” henceforth.)
Before I start, a small disclosure. In 2015, a colleague and I had a manuscript desk-rejected by Psychoneuroendocrinology for what we considered inadequate reasons. This led to a complaint to the Committee on Publication Ethics and a change in the journal’s editorial policies, but unfortunately did not result in our article being sent out for review; it was subsequently published elsewhere. My interest in the Russell et al. article arose for entirely unrelated reasons, and I only discovered the identity of the journal after deciding to look at it. So, to the extent that one’s reasoning can ever be free of motivation, I don’t believe that my criticisms of the article that follow here are related to the journal in which it appeared. But it seems like a good idea to mention this, in case the editor-in-chief of the journal is reading this post and recognises my name.
This article is getting a fair amount of coverage in the UK media today, for example at the BBC, the Mail Online, the Independent, and the Guardian (plus some others that are behind a paywall). The simplified story that these outlets are telling is that “chronic fatigue syndrome is real and is caused by [the] immune system” (Mail Online) and that the study “challenges stigma that chronic fatigue is ‘all in the mind'” (Independent). Those are hopeful-sounding message for ME/CFS patients, but I’m not sure that these conclusions are justified.
I was made aware of this article by a journalist friend, who had received an invitation to attend a press briefing for the article at the Science Media Centre in London on Friday 14 December. By a complete coincidence I was in London that morning and decided to go along. I was allowed in without a press pass after identifying myself as a researcher, but when I tried to get clarification of a point that had been made during the presentation I was told that only reporters (i.e., not researchers or other members of the public) were allowed to ask questions. This was a little annoying at the time, but on reflection it seems fair enough since time is limited and the event was organised for journalists, not for curious researchers with a little time on their hands. There were about 10 journalists present, from most of the major UK outlets.
You can get a summary of the study from the media pieces linked above (the Guardian’s coverage by Nicola Davis is particularly good). If you haven’t seen the media articles, go and read them now, and then come back to this post. There was also a press release. I suggest that you also read the Russell et al. article itself, although it does get pretty technical.
What did the study claim to show?
Here’s my summary of the study: The participants were 55 people with hepatitis C who were about to undergo interferon-alpha (IFN-Î±) treatment. The treatment lasted 24, 36, or 48 weeks. At five time points (at the start of treatment, than after 4 weeks, 8 weeks, 12 weeks, and at the end of treatment, whenever that was), patients were asked about their levels of fatigue and also had their cytokine levels (a measure of activity in the immune system) tested. These tests were then repeated six months after the end of treatment. Patients were also assessed for depression, stressful life events, and childhood trauma.
Interferon-alpha occurs naturally in the body as part of the immune system, but it can also be injected to fight diseases in doses that are much greater than what your body can produce. It’s sometimes used as an adjunct to chemotherapy for cancer. IFN-Î± treatment often has substantial fatigue as a side effect, although this fatigue typically resolves itself gradually after treatment ends. But six months after they finished their treatment, 18 of the 55 patients in this study had higher levels of fatigue than when they started treatment. These patients are referred to as the PF (“persistent fatigue”) group, compared to the 37 whose fatigue more or less went away, who are the RF (“resolved fatigue”) group.
The authors’ logic appears to run like this:
1. Some people still have a lot of fatigue six months after the end of a 24/36/48-week long course of treatment with IFN-Î± for hepatitis C.
2. Maybe we can identify what it is about those people (one-third of the total) that makes them slower to recover from their fatigue than the others.
3. ME/CFS patients are people who have fatigue long after the illness that typically preceded the onset of their condition. (It seems to be widely accepted by all sides in the ME/CFS debate that a great many cases occur following a infection of some kind.)
4. Perhaps what is causing the onset of fatigue after their infectious episode in ME/CFS patients is the same thing causing the onset of fatigue after IFN-Î± treatment in the hepatitis C patients.
Russell et al.’s claim is that patients who went on to have persistent fatigue (versus resolved fatigue) at a point six months after the end of their treatment, had also had greater fatigue and cytokine levels when they were four weeks into their treatment (i.e., between 46 and 70 weeks before their persistent fatigue was measured, depending on how long the treatment lasted). On this account, something that happens at an early stage of the procedure determined how well or badly people would recover from the fatigue that was induced by the treatment once the treatment was over.
Just to be clear, here are some things that Russell et al. are not claiming. I mention these partly to show the limited scope of their article (which is not necessarily a negative point; all scientific studies have a perimeter), but also to make things clearer in case a quick read of the media coverage has led to confusion in anyone’s mind.
– Russell et al. are not claiming to have identified the cause of ME/CFS.
– Russell et al. are not claiming to have identified anything that might cure ME/CFS.
– Russell et al. are not claiming to have demonstrated any relation between hepatitis C and ME/CFS.
– Russell et al. are not claiming to have demonstrated any relation between interferon-alpha, whether this is injected during medical treatment or naturally produced in the body by the immune system, and ME/CFS. They do not suggest that any particular level of IFN-Î± predicts, causes, cures, or is any other way associated with ME/CFS.
– Russell et al. are not claiming to have demonstrated any relation between a person’s current cytokine levels and their levels of persistent fatigue subsequent to interferon-alpha treatment for hepatitis C. (As they note on p. 7 near the bottom of the left-hand column, “we … find that cytokines levels do not distinguish [persistent fatigue] from [resolved fatigue] patients at the 6-month followup”.)
– Russell et al. are not claiming to have demonstrated any relation between a person’s current cytokine levels and their ME/CFS status. (As Table 2 shows, cytokine levels are comparable between ME/CFS patients and the healthy general population.)
Some apparent issues
Here are some of the issues I see with this article in terms of its ability to tell us anything about ME/CFS.
1. This was not a study of ME/CFS patients
It cannot be emphasised enough that none of the patients in this study had a diagnosis of ME/CFS, either at the start or the end of the study, and this greatly limits the generalisability of the results. (To be fair, the authors go into some aspects of this issue in their Discussion section on the left-hand side of p. 8, but the limitations of any scientific article rarely make it into the media coverage.) We don’t know how long ago these hepatitis C patients were treated with interferon-alpha and subsequently tested at follow-up, or if any of them still had fatigue another six or 12 months later, or if they ever went on to receive a diagnosis of ME/CFS. One of the criteria for such a diagnosis is that unresolved fatigue lasts longer than six months (it would have been really useful to have had a further follow-up). But in any case, the fatigue that Russell et al. studied was, by definition, not of sufficient duration to count as “chronic fatigue syndrome” (and, of course, there are several other criteria that need to be met for a diagnosis of ME/CFS; chronic fatigue by itself is a lot more common than full-on ME/CFS). I feel that it is therefore rather questionable to refer to “the presence of the CFS phenotype… for … IFN-Î±-induced persistent fatigue” (last sentence on p. 5). Maybe this is just an oversight, but even the description of persistent fatigue as “the CFS-like phenotype”, used at several other points in the article, is also potentially somewhat loaded.
Furthermore, the patients in this study were people whom we would have expected to be fatigued, at least throughout their treatment. IFN-Î± treatment knocks you about quite a bit. Additionally, fatigue is also a common symptom of hepatitis C infection, which makes me wonder whether some of the patients with “persistent fatigue” maybe just had a slightly higher degree of fatigue from their underlying condition rather than the IFN-Î± treatment — the definition of persistent fatigue was any score on the Chalder Fatigue Scale that was higher than baseline, presumably even by one point (and, theoretically, even if the score was 0 at baseline and 1 six months after treatment ended). So Russell et al. are comparing people who are recovering faster or slower from fatigue that is entirely expected both from the condition that they have and the treatment that they underwent, with ME/CFS patients in whom the onset of fatigue is arguably the thing that needs to be explained.
There are many possible causes of fatigue, and I don’t think that the authors have given us any good reason to believe that the fatigue that was reported by their hepatitis C patients six months after finishing an exhausting medical procedure that itself lasted for half a year or more was caused by the same mechanism (whatever that might be) as the multi-year ongoing fatigue in ME/CFS patients, especially since, for all we know, some or all of the 18 cases of persistent fatigue might have been only marginal (i.e., a small amount worse than baseline) or resolved themselves within not too many months.
2. Is post-treatment fatigue really unrelated to cytokine levels?
It can be seen from Table 2 of the article that the people with “persistent fatigue” (i.e., the hepatitis C patients who were still fatigued six months after finishing treatment) still had elevated cytokine levels at that point, compared to samples of both healthy people and ME/CFS patients. Indeed, these cytokine levels were similarly high in patients whose fatigue had not persisted. The authors ascribe these higher levels of cytokines to the IFN-Î± treatment; their argument then becomes that, since both the “resolved fatigue” and “persistent fatigue” groups had similar cytokine levels, albeit much higher than in healthy people, that can’t be what was causing the difference in fatigue in this case. But I’m not sure they have done enough to exclude the possibility of those high cytokine levels interacting with something else in the PF group. (I must apologise to my psychologist friends here for invoking the idea of a hidden moderator.) Their argument appears to be based on the assumption that ME/CFS-type fatigue and post-IFN-Î±-treatment fatigue have a common cause, which remains unexplained; however, in the absence of any evidence of what that mechanism might be, this assumption seems to be based mainly on speculation.
3. Statistical limitations
The claim that the difference in fatigue at six-month follow-up was related to a difference in cytokine levels four weeks into the treatment does not appear to be statistically robust. The headline claim — that fatigue was greater after four weeks in patients who went on to have persistent fatigue — has a p value of .046, and throughout the article, many of the other focal p values are either just below .05, or even slightly higher, with values in the latter category being described as, for example, “a statistical trend towards higher fatigue”, p. 4. But in the presence of true effects, we would expect a preponderance of much smaller p values.
Russell et al. also sometimes seem to take a creative approach to what counts as a meaningful result. For example, at the end of section 3.1, the authors consider a p value of .09 from a test to represent “trend-statistical significance” (p. 4) and at the start of section 3.2 they invoke another p value of .094 as showing that “IL-6 values in [persistent fatigue] subjects … remained higher at [the end of treatment]” (p. 5), but in the sentence immediately preceding the latter example, they treat a p value of .12 as indicating that there was “no significant interaction” (p. 5).
These borderline p values should also be considered in the light of the many other analyses that the authors could have performed. For example, they apparently had all the necessary data to perform the comparisons after eight weeks of treatment, after 12 weeks of treatment, and at the end of treatment, as well as the four-week results that they mainly reported. None of the eight-week or 12-week results appear in the article, and the two from the end of treatment are extremely unconvincingly argued (see previous paragraph). It is possible that the authors simply did not perform any tests on these results, but I am inclined to believe that they did run these tests and found not to provide support for their hypotheses.
There is also a question of whether we should be using .05 as our criterion for statistical significance with these results. (I won’t get into the separate discussion of whether we should be using statistical significance as a way of determining scientific truth at all; that ship has sailed, and until it voluntarily returns to port, we are where we are.) Towards the bottom of the left-hand column of p. 8, we read:
Finally, due to the sample size there was no correction for multiple comparisons; however, we aimed to limit the number of statistical comparisons by pre-selecting the cytokines to measure at the different stages of the study.
It’s nice that the authors pre-selected their predictors, but that is not sufficient. If (as seems reasonable to assume) they also tested the differences between the groups at eight or 12 weeks into the treatment, and found that the results were not significantly different, they should have adjusted their threshold for statistical significance accordingly. The fact that they did not have a very large sample size is not a valid reason not to do this, so I am slightly perplexed by the term “due to” in the sentence quoted above. (The sample size was, indeed, very small. Not only were there only 55 people in total; there were only 18 people in the condition of principal interest, displaying the “CFS-like phenotype”. Under these conditions, any effect would have to be very large to be detected reliably.)
I don’t find Russell et al.’s study to be very convincing. My guess is that different cytokine levels do not predict fatigue in either hepatitis C/IFN-Î± patients or ME/CFS patients, and that the purported relation between cytokine levels at four weeks into the IFN-Î± treatment and subsequent fatigue may well just be noise. In terms of explaining how ME/CFS begins, let alone how we might prevent or cure it, this study may not get us any closer to the truth.
11 thoughts on “Trial By Error: The New Interferon “CFS” Study”
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Great summary by my colleague. I flagged the irrelevance of this study up myself, immediately after publication, but me is female and perhaps perceived as the ‘elite’. We’re in an age where ‘elite’ and ‘expert’ has become a dirty word. Which doesn’t actually help anyone but there’s a lot of it about.
I’ll flag this up a last time. Anyone referring to the BPS model says little other than they don’t know basic psychology. One can see all illnesses, including norovirus but perhaps not food poisoning caught from eating in a restaurant, in terms of a BPS model. It’s not a particularly helpful model as a result. It’s not used by researchers into ME either. We refer to more specific issues like fear avoidance. Rejection of this terminology indicates a degree of group think by people not familiar with the subject or disinterested in accuracy. That reinforces the stereotype of the ill-informed patient/activist. It’s an own goal. To persist with it therefore doesn’t really help patients. Activists, review your motivation and if you are into group think and reject expertise cause everyone does, then maybe move on to something else. PWME need some serious, evidence-based arguments. Not terms that indicate non-scientific motives or simple rejection of all things psychological.
This does illustrate the significant influence of the Science Media Centre on the British and to a lesser extent the American press.
This research was presented to the world as answering significant questions about the nature of ME/CFS, and universally reported as such by the British press and BBC radio, when at best it is likely to become an interesting foot note in persistent or chronic fatigue studies. Also it is likely to prove a dead end, even if this so far unsuccessful attempt to use drug induced persistent fatigue in patients with an existing infection, ie Hepatitus C, did turn out to provide a relevant model for the acquisition of ME/CFS. Interferon-alpha is increasingly being superseded by other drugs as a treatment for Hepatitus C without the current side-effect, making any future better designed studies on this issue unlikely.
This study raises more questions than it answers:
– What was the immune status of these Hep C patients, prior to their acquisition of Hep C? (This is relevant in that the suggestion is that the immune status at the time of the persistent fatigue being triggered is a factor in it becoming chronic, which for actual ME/CFS patients is presumably, in those whose ME/CFS is triggered by an infection, at the point that healthy individuals acquire the infection. But we know nothing of the Hep C patients’ immune status prior to their acquisition of Hep C.)
– What percentage, if any, of Hep C patients are likely to acquire more robustly defined ME/CFS as a result of the infection, regardless of any Interferon Alpha treatment? (Given a range of infections and possibly even inoculations, amongst other ’causes’, can trigger trigger ME/CFS, we can not rule out the possibility that some in the study did have ME/CFS regardless of the Interferon treatment.
– What is the wider symptom profile of the Hep C and the so called ‘CFS’ patients? (This study looks at the one dimension of fatigue and used the now widely discredited Oxford criteria, requiring only six months of persistent fatigue, to define CFS. However internationally it is accepted that the Oxford criteria produce a very heterogenous group that unhelpful confounds the symptom of chronic or persistent fatigue with the condition chronic fatigue syndrome which has many other symptoms included the core symptom of post exertional malaise. Did any of the Hep C patients with persistent fatigue display any of the other ME/CFS symptoms including PEM and did any go on to be diagnosed with ME/CFS?)
– How many, if any, of the ‘CFS group’ in this study actually had ME/CFS defined by more robust criteria? (Given it is widely accepted that immune abnormalities are a feature of ME/CFS, how might a more appropriately defined comparator group of ME/CFS patients compare to the Hep C persistent fatigue group.)
– What happens to the persistent fatigue Hep C group longer term? (The suggestion that immune status at the time of the trigger is the reason for the fatigue symptom becoming chronic in the absence of an ongoing biomedical cause, would seem to imply one would expect the condition to be stable or to resolve. However this is not necessarily characteristic of ME/CFS, which can be stable or improving, but also can be relapsing/remitting or even progressively deteriorating.)
It is so frustrating that the exclusive focus on the one symptom of fatigue and the use of an outdated criteria to define ‘CFS’ that also focuses just on fatigue, means any potential usefulness of this study meaningfully comparing persistent fatigue in Hep C patients with ME/CFS was lost.
This suggests that the researchers do not understand the reality of ME/CFS, but also raises the question why did the Science Media Centre so vigorously promote this one study that tells us little about ME/CFS out of the dozens, if not hundreds, of more relevant studies into the various biological dimensions of ME/CFS published annually?
It is positive that the casual reader hopefully takes away from this press coverage an understanding that ME/CFS is a real biomedical condition, but it is hardly the major breakthrough into the understanding of ME/CFS that the publicity would have us believe.
Ellen, since you have offered your point of view, I will offer you mine.
The CBT/GET model and the BPS brand are not based on sound science but on eminence, persuasive rethoric, and bad research practices like p-hacking that creates the superficial impression that there is some scientific foundation to what is being done.
Supporters of the CBT/GET model and BPS brand typically respond to criticism by belittling or ignoring the critics. This only reveals that you do not have any counterarguments to the criticism. Can you explain why someone should consider studies as reliable when they are unblinded, involve therapies that attempt to change how patients see their symptoms and illness, rely on subjective outcomes, and have inadequate control groups as reliable? No, you cannot. Can you point to any study that unanbigously establishes that CFS is perpetuated by psychological factors? I doubt you can.
It is true that CBT/GET and the BPS brand are now widely opposed and even hated. That is merely the consequence of the continued dishonesty and incompetence of its proponents that appear unable to accept that their cherished beliefs are simply wrong.
The global media coverage of this research is not about the research.
It is about a group of people who have built their careers, reputations and bank accounts on their particular spin of the BPS model and their particular ‘treatment’, and are positioning themselves for further gains.
It is about orchestrating unfounded media coverage – again – to control the global ME narrative and to preserve their power in the light of overwhelming biological evidence – and at the expense of many millions of people living with ME world wide.
It is about the continued monetization of their egos – and of institutionalized medical harm.
Do we need to coin the term biopsychobabble?
Also replying to Ellen. My psychiatrist report in advance of the sessions, who did my CBT stated it was to fix and I quote ‘false illness beliefs’. Would you like to explain to me what false illness beliefs we suffer from as a group? And what evidence is there for that ridiculous notion?
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But….. for all that the Russell et al team are not claiming, the SMC briefing, newspaper articles, headlines and interviews about this study DO link the study results to CFS/ME. And this should be a big positive for patients with ME/CFS. (Bear with me).
In a BBC Radio Wales interview about the study, Professor Pariante answered a question put by a patient by indicating that there was a â€˜clear distinctâ€™ between depression or other mental health problem and the development of chronic fatigue in patients in the study. But CFS/ME patients in the UK are now being directed by the NHS to the IAPT psychotherapy programme where they are treated with CBT and GET. Those who accept this IAPT treatment are ALL coded with the â€˜somatization disorderâ€™ code ICD-10 F45.0 as their ‘problem descriptor’. Either this study is relevant to patients with CFS/ME and this finding is too, or it is irrelevant. Which is it to be?
Given that the IoPPN apparently rates this study very highly and seems convinced about its relevance to patients with CFS/ME then, on the basis of this study and its authorâ€™s remark, this institution surely has a duty now to petition the NHS and Government to stop this coding for ALL CFS/ME patients and apologize for the appalling way in which patients have been treated and dismissed by the NHS to date.
Aronowitz (Making Sense of Illness) and Pinch (Chapter 5 of Dr. Golem) present the BPS model, leaving out any reference to social and economic factors such as the wish of medical insurers, including the DWP to minimise their expenses by keeping ME/CFS labelled a psychiatric complaint, which only attracts disability payments for two years rather than for life if it is labelled a medical (the â€˜bioâ€™ bit of BPS). These institutions are prepared to pay well for the services of psychiatrists who can maintain the psychiatric label, and the UK psychiatrists who do this work have income and reputation to lose if they lose this battle. Yes, there is rather a lot of biopsychosocial effect going on.
Itâ€™s interesting how influential Simon Wessely has been with women who write books. Elaine Showalter, the author of Hystories, which describes (in an only somewhat hysterical tone) how the modern world is succumbing to a dangerous wave of hysteria and can only be saved if we all recognise that we need psychotherapy, starts off with extensive praise for the advice and help she has received from the â€˜medical historianâ€™, Simon Wessely. Her book became a very popular and influential best-seller in the late 1990â€™s, offering invaluable support to the â€˜mass hysteriaâ€™ school of thought, thereby doing inestimable harm to people with ME. She explains that people get ME because they read descriptions of it in the press and decide they have it. (This suggests that the Icelandic school-boys from a remote village who suffered an outbreak must have had unusual and exclusive access to the U.S. popular media!)
Recently, the Wellcome Prize, which is for literature with a medical theme, but specifically not for case studies, was awarded to a book called â€˜All In Your Headâ€™. this was a series of case studies masked as literature by the simple device of not including an index or set of references. The author also acknowledges support and encouragement from Professor Wessely, who happened also to have an advisory relationship with the Wellcome Foundation.
Oh, and he is also on the board of the Science Media Centre.
This recent article has a distinct whiff of â€˜if you canâ€™t lick â€˜em, join â€˜emâ€™. II agree with the prediction that CBT/GET will be found to be curative of whatever these problems are supposed to be.
(And while Iâ€™m here, could we please stop talking about â€˜fatigueâ€™ and start taking about â€˜muscle failureâ€™? Everyone gets tired, not everyones muscles just stop working when they walk across a room. It would clarify things a whole lot, especially when we also stop saying that people who are depressed suffer â€˜fatigueâ€™. They donâ€™t have â€˜fatigueâ€™, they have â€˜apathyâ€™. It is not hard, at all, to distinguish ME/CFS from depression, unless you really donâ€™t want to.)
Yes, there is quite a lot of â€˜psychosocialâ€™ stuff going on in relation to ME/CFS!
I will leave the statistical analyses to others who are much, much (much) better than I at them and instead just point that interferon induced fatigue prompted perhaps the first understanding that the immune system and the brain were producing fatigue and other symptoms during infection not the pathogen.
Andrew Miller has found that interferon treatment produces essentially the same changes in the brain in severely fatigued hepatitis C patients and people with ME/CFS. These changes involve basal ganglia – a part of the brain involved in movement, reward and fatigue.
In fact, the biological investigations into the causes of interferon induced fatigue, psychomotor slowing (also found in ME/CFS), sleep problems, etc have been extensive and very illuminating! Check out some of Andrew Miller’s work here – https://www.ncbi.nlm.nih.gov/pubmed/?term=interferon+hepatitis+c+fatigue++miller
And the basal ganglia work he’s done in ME/CFS is fascinating. https://www.healthrising.org/blog/2014/09/15/unrewarding-reward-basal-ganglia-inflammation-fatigue-chronic-fatigue-syndrome/
The most interesting part, for me, though, is the possibility that inflammation prompted by interferon, or in the case of ME/CFS, by a pathogen, is able to knock out a part of the basal ganglia which produces dopamine – which then renders the system hypersensitive to further inflammation – thus presenting a potential model of not only hypersensitized microglia – which Younger believes in present in ME/CFS – but a viable way of explaining the problems with physical activity.
Miller’s work, unfortunately, was not referenced by the English group. Hopefully that group won’t use the results to argue for more CBT/GET. I don’t know they would. This study found no evidence that psychological factors played a role at all.
Given the rich biological vein that’s been opened by the hepatic C/Interferon studies hopefully future studies by this group will continue to mine that part of it.
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