MrMagoo
Senior Member (Voting Rights)
Seems like you’re trying to apply logic to nonsense!
Criticisms of DecodeME in the media - and responses to the criticisms
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MrMagoo
Senior Member (Voting Rights)
But he didn’t say FND is ME, he said ME is like it’s a functional disorder, you see. He didn’t say which functional disorder.
Some of you are too tied to the idea of facts, and things “making sense” and Alan spouting BS! Classic Functional Making Sense Of Things Disorder.
Jonathan Edwards
Senior Member (Voting Rights)
That is one argument - and valid.
But the other argument is also valid - that the 'ME/CFS/' cohort contained a significant number of people with some other problem with a genetic basis. The main argument against this is that the genes pulled out by DecodeME are not picked out in conditions likely to cause interference. The pain gene may be the same variant picked up in fibromyalgia but that would be a not unexpected overlap.
Yann04
Senior Member (Voting Rights)
You find similarly high rates in ME if you look at twin heritability studies.
And similarly modest ones to decodeME if you look at GWAS heritability in depression and anxiety.
Fundamentally he’s weaponising two very different ways to measure heritability. It’s like comparing degrees celcius to degrees farenheit.
Hoopoe
Senior Member (Voting Rights)
What would Carson make of the observation that the following things are typical of ME/CFS but not typical of depression?
Having to lie flat at least some of the time
Delayed worsening of symptoms in response to activities
Rest in a quiet, darkened room improves symptoms.
Can have significant functional impairment and symptoms with normal mood, for long periods of time.
PEM episodes follow a very different time pattern than depressive episodes.
The healthcare system is oriented towards detecting certain symptoms typical of depression, but has not been trained to look for certain problems typical of ME. When one only looks at things like fatigue, sleep issues, cognitive impairment ME/CFS does resemble depression, but when other things are considered it begins looking different.
Having to lie flat at least some of the time
Delayed worsening of symptoms in response to activities
Rest in a quiet, darkened room improves symptoms.
Can have significant functional impairment and symptoms with normal mood, for long periods of time.
PEM episodes follow a very different time pattern than depressive episodes.
The healthcare system is oriented towards detecting certain symptoms typical of depression, but has not been trained to look for certain problems typical of ME. When one only looks at things like fatigue, sleep issues, cognitive impairment ME/CFS does resemble depression, but when other things are considered it begins looking different.
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Some depressive co morbidity is to be expected in long term illness. Open question as to whether it worsens non depressive features. My bet is that any study of , say, MS. or sarcoid will cover numerous with depressive states.
Depressive co-morbids in the absence of genetic signatures for depression strengthens the argument against depression as initiating factor at least. The more the merrier. For a Prof of NPs I would think this would be an obvious immediate observation.
I think the question as to constitution of cohort is valid and I wonder whether I as a sarcoid sufferer with a fatigue state illness well established before sarcoid diagnosis have shown the ME signature or not.
I think there is a difference between conceptualisation and what is going on bilogically in individuals. So, C might focus on stress handling and a few of Garner's Recovery crew might fit in there, but even the Recovery crew allow that the kind of biophysical aspects addressed by Alex Howard's clinic are varied , that treatment may be necessary and such aspects may be making people sick by direct mechanisms and as general stressors.
Why " ME is a FSD" rather than "FSD is found in ME"?
Some posts have been moved to this thread:
General news about Fabricated and Induced Illness syndrome (FFI)
General news about Fabricated and Induced Illness syndrome (FFI)
Jonathan Edwards
Senior Member (Voting Rights)
Another one who needs to go and boil his head.
Barry
Senior Member (Voting Rights)
Moved posts
Another question here, this time more of a devil's advocate one.
To be very clear, I do not in any way believe ME/CFS is a psychological condition whatsoever, my wife (who is the ME sufferer) having demonstrated that day after day for many years.
But it occurs to me the psych brigade could try to argue this study does not disprove anything of theirs, and I would like to understand what the counter argument to that would be.
The GWAS basically shows that ME/CFS sufferers have a genetic predisposition towards suffering from the condition. But what if the psych brigade simply argue: "Well, all that shows is they have a genetic predisposition to having unhelpful beliefs". What is the counter argument to that? Are there mental/behavioural conditions that might show a genetic predisposition to?
Again to emphasise, I do not believe that in the slightest, I know it not to be the case. But I would like to understand.
Edit to clarify: As my post has been moved to the "Criticisms of DecodeME in the media - and responses to the criticisms", I would just like to clarify that this post of mine is not a criticism at all, simply a request for further understanding. The whole point is that I don't understand the issue enough to even make such a criticism
.
Another question here, this time more of a devil's advocate one.
To be very clear, I do not in any way believe ME/CFS is a psychological condition whatsoever, my wife (who is the ME sufferer) having demonstrated that day after day for many years.
But it occurs to me the psych brigade could try to argue this study does not disprove anything of theirs, and I would like to understand what the counter argument to that would be.
The GWAS basically shows that ME/CFS sufferers have a genetic predisposition towards suffering from the condition. But what if the psych brigade simply argue: "Well, all that shows is they have a genetic predisposition to having unhelpful beliefs". What is the counter argument to that? Are there mental/behavioural conditions that might show a genetic predisposition to?
Again to emphasise, I do not believe that in the slightest, I know it not to be the case. But I would like to understand.
Edit to clarify: As my post has been moved to the "Criticisms of DecodeME in the media - and responses to the criticisms", I would just like to clarify that this post of mine is not a criticism at all, simply a request for further understanding. The whole point is that I don't understand the issue enough to even make such a criticism
.
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"Great, maybe people with ME/CFS have a genetic predisposition to unhelpful beliefs. Unfortunately, none of the treatments you have suggested have worked, so lets examine the specific mechanisms through which these genes cause ME/CFS. The genetics seem to be pointing to people with ME/CFS having something different about genes in the brain, so lets see if we can figure out what specifically is physically different in the brain or elsewhere to try to come up with a treatment."
Kitty
Senior Member (Voting Rights)
My response would be that they'd use the same tactics whatever DecodeME showed.
Literally, it could have turned up that we're all from bloody Venus and they'd still find ways to say it's the result of unhelpful beliefs. I think we should stop worrying about them; they're beyond help.
There are people who currently share their viewpoint in the sincere belief there's an evidential basis for it, and they're probably not beyond help. They're misinformed rather than indoctrinated, and when we have a clearer story we should do our best to make sure they hear it.
Jonathan Edwards
Senior Member (Voting Rights)
Genes might predispose to beliefs through a biological mechanism. No problem. (Genes might predispose someone to the belief that they are weak if the genes encode for muscular dystrophy.)
But perhaps the strongest conclusion one can draw from PACE is that beliefs are not the problem in MECFS. So they are not unhelpful. The trial showed that you may be able to talk people into thinking differently about their health, or at least talking as if they did, but it makes no difference to more objective measures of how they are. They didn't get better. So the flaw in the argument is the invocation of unhelpful belief.
The BPS approach pivots on the idea that you can separate 'psychological' and 'social' causation from biological causation. Note that depression that is not explained as a reaction to circumstances is called "biological". Psychiatrists treat it as such. But "psychological" in the BPS sense is not psychiatric or mental, it is some causation that can be treated as outside biology. Genes are biology. So we expect biological depression to link to genes. We can also reasonably expect genes to determine how miserable someone becomes after being made redundant or losing a loved one.
But that still doesn't make reactive depression fit "BPS". Nobody is likely to say that your depression "is psychological" in a BPS sense. The BPS guru does not claim that someone isn't really depressed, and just have this mind set that they are miserable when really they are a bundle of fun. The psychodynamic therapist might claim that you believe everything is terrible when in fact it is fine and that that is the problem. But most of us in medicine long ago went over to the view that having an abnormally negative take on things is driven by biology - neurotransmitters, synapses, and so on.
If BPS people start scoffing at DecodeME and saying that, so what, lot of psychological illnesses show gene links, what I would say is that what they mean is psychiatric illness And if they are suggesting that MECFS is on a par with those why are MECFS patients dying of starvation because they are denied feeding support because their illness is seen as not psychiatric but functtional or biopsychosocial. Why do people with psychiatric disorders get full on long term care and life support when MECFS patients are just sent home to die?
Whether or not MECFS is a psychiatric illness doesn't depend on causation, it depends on the presentation of the illness. And by and large we can say pretty clearly that it is not psychiatric because it does not involve disordered thought in the way that neuroses and psychoses do but, for instance, dementia and Parkinsonisn do not. It is not an illness of derangement, but it does interfere with people's cognition. So it isn't a psychiatric disorder and never looked like one. Whether it is a bioposychosocial disorder is a completely different question, which does depend on what you believe about causation, and one which PACE answered with a fairly clear No.
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Barry
Senior Member (Voting Rights)
Yes, my wife exemplifies this. And you are right, her beliefs are fine, the key point is that they align with her very real condition, nothing unhelpful about them at all. Sensible pacing relies on this. And I've said before, she always does as much as she can, never as little.
I suppose the point is that the genetic anomalies are indisputably physiological anomalies, no matter what their manifestations or what part of the body point to.
Jonathan Edwards
Senior Member (Voting Rights)
And perhaps that depression is also indisputably physiological and those who use BPS explanations and treatments have no business to be managing depressed people either.
Dolphin
Senior Member (Voting Rights)
Response to DecodeME Preprint
"The DecodeME study is the largest of its kind to date, but its findings need careful interpretation". Read the full statement from COFFI researchers and consumers!
www.coffi-collaborative.com
- 15 hours ago
Response to DecodeME Preprint
Statement from researchers and consumers from the Collaborative on Fatigue and related symptoms Following Infection (COFFI)
The DecodeME study is the largest of its kind to date, but its findings need careful interpretation. They are not a groundbreaking, and we are concerned with the way these preliminary findings are being promoted. Once replicated, they may be another piece of the puzzle in understanding mechanisms behind ME/CFS.
Background
We know the condition is real and our genes are implicated
1. We recognise the need for high quality research to better understand the underlying biological mechanisms in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).
2. A recent genetics analysis in people with ME/CFS was made publicly available as a pre-print prior to peer review. This research is a helpful contribution to the knowledge base. The researchers sought genetic markers associated with the condition through a genome-wide association study (GWAS). This study, called the DecodeME project, has attracted press headlines and many contain strong statements from the study authors, for example:
“These results are groundbreaking. We have gone from knowing next to nothing about the causes of ME/CFS to giving researchers clear targets.” (Sonya Chowdhury, author).
"For so long people with ME/CFS have been told it's all in their head. It's not. We see it in their blood." (Chris Ponting, senior author).
3. The messaging has created widespread excitement and raised expectations in both the research and patient communities. The research has been presented as ground-breaking and heralding an imminent cure.
COFFI response
4. The researchers of the Collaborative on Fatigue and related symptoms following Infection (COFFI – www.coffi-collaborative.com) and their Consumer Advisory Group (CAG) were surprised by the hyperbole in reporting the findings. COFFI researchers and consumers have recognised this condition as real for more than 25 years and recognise that the research into the genetic link has long been established, although perhaps not with specific predisposing genes implicated.
5. In the light of these concerns, the COFFI consumer advisory group and the COFFI researchers provide a commentary.
COFFI consumers’ commentary
Views on the hyperbole
6. The effort put in and the size of the study is impressive and this adds useful knowledge. However, the study authors state that showing an association with genes somehow demonstrates that the condition is “real”. This is not particularly useful, because we already recognise the condition is real.
7. Genes are part of the picture, but there is a danger with this emphasis. The statement “we see it in the blood” implies for consumers that genes “cause” the condition. This statement may contribute to some patients believing nothing can be done unless we get a biomedical cure.
8. This narrative may lead them to believe the condition cannot be influenced by approaches based on a biopsychosocial approach, which is clearly helping many people to reduce symptoms and some to recover.
9. The hyperbole around research showing genes influence risk in ME/CFS has happened before: 20 years ago a press release stated that researchers were close to finding the genes responsible for ME/CFS, and that they expected to have treatments within a year. At that time, patients waited for a cure, but nothing appeared, and patients deteriorated in the meantime making recovery harder.
Research on practical measures that help needed
10. The article states there are no effective treatments, but this is incorrect. There are a range of strategies for rehabilitation, drawing on the biopsychosocial explanation of this condition. These include cognitive behaviour therapy, approaches to safely increase activity and mind-body approaches. The research indicates these options may help people reduce symptoms and ensure some recover. Putting patients on hold with this condition awaiting a drug could be unhelpful.
11. We also know that recovery is possible, and question why recovered patients were not included in the genetic analysis. Maybe this is a question to be added in further research. It would be interesting to know whether genetic, environmental, or psychological factors influencing the occurrence, severity and chance of recovery.
12. In summary, the Collaborative consumers noted the emphasis on genetics does not help people currently with the condition. Genetic studies can expand understanding, but people with ME/CFS also need practical answers now. Research into treatments, rehabilitation, and support strategies must remain a priority.
COFFI researchers’ commentary
Findings interesting but not ground-breaking
13. The COFFI researchers considered the study. We note its size, and that the genetic traits related to brain and immune function, which supports what we already know.
14. We all recognize that persistent fatigue, like many conditions (including cardiovascular disease and depression) has a genetic component, so genes can influence risk of developing the condition. We also know that this genetic contribution to risk is likely not to be from one gene but from several (“polygenic”).
15. We note that the eight genetic markers reported in the pre-print were associated with the condition, but the size of the effect found were modest. This means that the same genetic markers were also present in many healthy control participants. This makes their isolated interpretation limited. Further analysis looking at various gene combinations may be more informative.
16. Like other conditions such as heart conditions or depression, the heritable component, the genes, are only one influence on the risk of developing the condition. Most human illnesses result from very complex interplay between many genetic factors, and things that people are exposed to throughout their life.
17. We also know that genetic influences can be altered by environmental exposure. This phenomenon, known as epigenetics (how our environment can switch genes on or off), was not examined.
Patients varied, and the study requires peer review and replication
18. We note that the ME/CFS diagnosis was based on self-report. This means the patients will be quite varied, and only a small minority reported onset with a documented infection, whereas fatigue conditions can arise because of many different precipitating causes. This wide variation in the patients may well lead to flawed positive associations with genes that have no influence; and on the other hand, may miss actual associations.
19. The findings are yet to be peer reviewed, which may alter the interpretation, and all good science the analysis needs independent replication. The DecodeME researchers themselves state they were unable to identify the specific genetic markers in other large data samples they had access to and this is important.
20. In summary, this large study has some interesting findings with specific genes identified. This is a contribution to what we know already, and needs replication.