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Mind/Brain and ME theorising

Marco

Grrrrrrr!
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2,386
Location
Near Cognac, France
We have also ignored one key aspect. While connections may exist, they may not be activated. Non activation of connections (which in some cases may dwindle or die) is also important. Edelman posited that deep emotional centers of the brain (he allowed for a range, we was mainly concerned with end mechanisms)could send signals that change the response capacity of the synapses toward or away from change the strength or type of connection. Much of what we consider to be learned survives, in my interpretation of his view, only because their is no sufficient signal to trigger synaptic plasticity.

Just as an aside, or as a general point, there's a tendency to talk largely in terms of inputs activating connections which then activate others etc but less about the role of inhibition. I've a sneaking suspicion (which I can't of course prove) that much of the brain's activity (and hence energy consumption) is involved in inhibition rather than activation.

When I published one of my earlier blogs on HR, which was basically positing that ME/CFS involves deficit in sensory inhibition based of a variety of 'converging evidence' (the proposal was simplistic involving excitatory/inhibitory neurotransmitters but can easily be accommodated in terms of microglia) someone (an MD no less) sent me a paper to read. It turned out to be a sceptic's demolition of some elaborate theory of how near death experiences were 'proof' of life after death. I was a little offended as I thought the point they were making in sending me the paper was how easy it is to build a house of cards but the point was taken.

But it was an interesting enough read and after re-reading the paper concluded that near death experiences (the tunnel of light, whole life flashing before you) may be readily explained by the breakdown of the dying brain's inhibitory mechanisms.

In terms of encoding of experiences, inhibitory mechanisms may play the role of data compression?
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Out of interest do you remember what the mistakes in Feynman were?
Why do you think QM needs no interpretation?

I thought someone would ask that so i have got vol III out and am trying to find the mistakes.

Feynman start chapter 1 very well with the idea that it is simply wrong to try to think of quantum dynamic units in terms of what we are used to. They are not particles and they are not waves. I think he dilutes his message later by saying that we might call them particle-waves and that the particle story is sometimes right and the wave story is sometimes right. Leibniz is much better in his description of fundamental dynamic units - they have 'no extent nor figure'. They are simply not imaginable at all in familiar terms. This is why there are no interpretations of QM - interpretations are only ever attempts to imagine 'what the quanta are like' - maybe as particles with pilot waves or 'process 1 and process 2'. Leibniz saw that this was not just forbidden for some arbitrary reason but forbidden because of a logical necessity relating to indivisible dynamic units. To be indivisible is to have no parts that could be features or appearances.

Feynman reveals his half-heartedness in chapter 1 by saying quantum mechanics is about small things. Leibniz is better - these fundamental units have NO SIZE AT ALL. In fact their wave equations give values for everywhere in the universe throughout time. If they have any size it is the size of everything that ever was or will be. They connect at specific places but they are not small. Feynman himself points out that a bullet can be treated as a quantum unit - it will show interference, except so tiny that it would be unmeasurable. We now know that the biggest things we can possibly measure interference for - at present buckminsterfullerine molecules - do show diffraction rings.

Feyman actually goes into the phislosophers' lion's den in chapter 2.6. He makes the mistake of saying that measurements affect what is measured. Leibniz knew that this is flawed - causal statements of this sort go out of the window once we are talking fundamental reality. Otherwise he says a lot of sense, particularly about the silliness of relating quantum randomness to free will. He makes a small error in relation to what the mind would seem like in a classical world - because it couldn't seem like anything - which is why Leibniz realised we needed another level, which became QM. But that is pretty small print.

Last time I read it I think I might have had other grouses but that is what I see now!
 

Jonathan Edwards

"Gibberish"
Messages
5,256
So to me an image is literally the image that is what ever is picked up on sensors (neural signals from cones and rods in the eye, or for a computer the signal from the sensor chip). The representation of objects as you suggest and as I would agree is an internal representation of the content of the image which is different (and much more compact!). With language describing physical relationships of objects there are examples where people don't remember the detail of what is specified in the sentence but the consequential relationships between objects. I suspect there is similar work looking at images and image processing but have never looked.

Most people in neuropsychology seem to agree that there is no 'image' at the retina, but there is a lot of confusion about this. A pinhole camera produces an image on a white screen in a dark room because the screen reflects light like a picture - which can also be called an image. But the retina does not reflect an image - except maybe in a cat with a tapetum. All these usages have implications about an observer hidden in them somewhere and when you start getting an 'observer-free God's eye view descriptio' you tend to get problems. The classic issue is the false problem of the 'homuncular regress' attributed to Descartes's model. There is no regress if one reads Descartes properly. He understands that the input to the soul is not optical so there is no 'screen'.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Just as an aside, or as a general point, there's a tendency to talk largely in terms of inputs activating connections which then activate others etc but less about the role of inhibition. I've a sneaking suspicion (which I can't of course prove) that much of the brain's activity (and hence energy consumption) is involved in inhibition rather than activation.

There are indeed inhibitory fibers. Its not suspicion. I am speaking from 1995 neuroscience though, things change. It was integral to my neural model that you can have excitatory and inhibitory fibers. I think the visual cortex uses them. My science on this is waaaaayyyy out of date though.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
In terms of encoding of experiences, inhibitory mechanisms may play the role of data compression?
My understanding of inhibitory mechanisms is they prevent spread of signal. They localize signal, by suppressing surrounding signal. I could be wrong about this one point, but I think its critical to things like edge and line and form detection in the visual cortex.

In artificial neural networks they allow for synapses etc to go from positive to negative etc. I think that in many cases, if not all, connections are either activating or inhibitory. Again, 1995 science, which might not be up to date. However I cannot see that the chemistry allows for a synapse to change from inhibitory to excitatory or visa versa.

In artificial neural networks you get data compression by channeling signal through smaller and smaller areas. Its a function of the connectivity pattern. I am very not sure if this is the case in the brain. The complex architecture is much messier.

PS In artificial neural networks if you compress data you lose data, but you can gain a capacity to generalize. One risk here is that instead of generalizing you may memorize the data set. If you then test it with new data it fails. The brain does not appear to operate like this in general, but one wonders about dogma. ;)
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Just as an aside, or as a general point, there's a tendency to talk largely in terms of inputs activating connections which then activate others etc but less about the role of inhibition. I've a sneaking suspicion (which I can't of course prove) that much of the brain's activity (and hence energy consumption) is involved in inhibition rather than activation.

As I understand the current popular view (right or wrong) inhibition plays a dominant role in 'thinning out' incoming data. Cells tend to send positive signals to cells in other regions - for instance primary visual cortex sending stuff up to temporal/parietal areas for higher level analysis. But they connect to nearby cells mostly through inhibitory signals. The simple interpretation of this is that each area operates a bit like a Dutch auction room. Signals come in until one cell decides to fire - to bid as the auctioneer gradually lowers the price. As that firing occurs and sends excitatory signals to higher regions the same cell sends powerful inhibitory signals to all its neighbours. Effectively the auctioneer's hammer comes down and no more bids are allowed. The point of this is that at any instant there are far too many sensory inputs to think about so the system has to weed out the most salient until there is just one pattern that gets through to awareness.

By analogy with B cells (as usual) only the most specific B cells get expanded during an infection. Any cells a bit slow to bind are told to die. And in autoimmunity that selection fails for certain clones. In lupus selection fails across the board. I think it is not unreasonable to suggest that in ME this filtering process might be skewed. I doubt it is a purely quantitative thing. If you do not have inhibition at about the usual level you probably get seizures - everything starts exciting everything else. But collateral inhibition might fail in a more subtle way in nociceptive pathways.
 

lansbergen

Senior Member
Messages
2,512
I said I lost my memory but if that was true it could not have come back. It is more likely that I lost the ability to access stored information necessary for recalling it. I have a simple explanation for myself. Routes were physical blocked and when the obstacles were removed one by one my memory slowy came back.
 

Woolie

Senior Member
Messages
3,263
Snow Leopard said:
What are the common biases?

Last installment, but some of the real biggies here....

Multiple Comparisons and ROI’s

Another problem that arises in functional neuroimaging research is that fMRI collects so much data. No-one can interpret it all. Researchers do a few things to correct for this. First, they use statistical corrections (a bit like Bonferroni if you know that), so that only activation in areas of the brain that are marked and highly statistically reliable get reported.

But another thing happens sometimes too. The researchers focus on a “region of interest” (ROI), and look only at that. This is helpful statistically, as you don’t produce as many statistical results and you don’t have to statistically correct to such a degree, so you’re more like to find significant stuff, at least in your region of interest (ROI). But there’s a cost: you simply ignore any differences in other areas – handy for results that might be troublesome for you to explain or might go against your hypothesis.

Most studies do both a whole brain and a ROI analysis, so you can see the pro's and cons’ of both – but watch for those that do just the ROI one.

The tricky business of hypothesis testing.

A bigger problem: you can use functional neuroimaging to test a hypothesis about brain activity But you can’t use it to test a psychological hypothesis.

An example of this conundrum was published a few years ago. It was a case study of someone with “hysterical” leg weakness (their word not mine!). Some really clever researchers (who should have known better) found heightened activation in the anterior cingulate when this person was asked to try and move her bad leg. Since the anterior cingulate has been associated with effortful control, they argued this activation demonstrated an active effort to inhibit leg movement. Hey presto – hysteria confirmed!

But this type of activation is also observed whenever a person is faced with an especially challenging task – like, er, perhaps moving a leg that is not functioning properly?

The problem: you’re jumping levels of description. They don’t map one-to-one onto each other. There could be multiple psychological explanations for such activation differences. Its the problem of reverse inference all over again.

The confusion of cause and effect.

A huge problem with interpretation of functional neuroimaging studies of special populations – especially in the media – is that anything observed is often assumed to be the root cause of whatever ails that population.

Take the example of the amygdala in psychopaths. There have been a few studies showing that people who meet the criteria for psychopathy respond differently to pictures of people in pain or being hurt than non-psychopathic prisoners. The amygdala, a region known to be involved in emotional processing, is underactivated in these individuals during this task (usually in these studies, it’s a subtraction design so they compare activation in this task with a “control” or “baseline” task). It has been claimed that such studies demonstrate that psychopaths have a brain aberration which renders them unable to empathise.

But this makes no sense. Psychopaths, by definition, do not feel distress when other people are hurt. This is how the condition is defined. So its not at all surprising that brain regions such as the amygdala, which are known to be activated when people feel distress, are not as highly activated in these people when viewing others' pain. It’s a no-brainer (sorry, couldn’t resist:snigger:). In this study, the neural correlates are just that, neuronal correlates, not causes.

The best way to think of functional neuroimaging measures – especially ones that compare activation in at least two active tasks – is as another type of response, in the same general group as reaction time measures, self-report scales, etc.. Okay, they don’t involve action in the real world, and they’re not controllable by the person in quite the same way, but when it comes to interpretation, they're responses. They can be really useful measures in this way. They are a lot richer than, say response times, because they don’t just have one dimension – either fast or slow – they also have a second dimension: location. Plus it’s a new measure, and we could do with some better ones (self-report, well we know that one sucks). But its still pretty much a response.

Psychopaths don’t have brains that are “hard wired” to render them unempathetic (at least as far as we know). They are simply unempathetic, and their brain responses, like their verbal responses and their behaviour, are consistent with this. The neuroimaging data have no privileged status (see below). If you wanna test the causal role of the amygdala in psychopathy, you need a totally different method. For example, take a group of patients with amygdala dysfunction/damage due to a known condition (or damage to other regions implicated, like the orbitofrontal cortex). Are these people psychopathic? If so, it might suggest a causal role. But it turns out they're not.

So if someone’s proposing to use functional neuroimaging to study a special population (emphasis on functional here, structural imaging is another thing), don’t think biomedical study, think psychological study. Because most of the time, that’s exactly what it is. The brain activation is used as a measure of response to some set of stimuli or scenarios and the question is how this response differs from controls. The whole kit and caboodle is interpreted in psychological terms.

The “privileged status” fallacy

This one is kind of related to the last – it’s the idea that if we can describe behaviour in neuronal terminology, the implications somehow change. This is the concern I was talking about on the main thread when people confuse levels. Its illustrated nicely in the psychopath example above. Somehow the psychopaths don’t seem as responsible for their behaviour any more, now we know it goes on in their brain. But think about it: Of course if goes on in their brain – where else would it be?

I worry about this with ME because people think fMRI findings will demonstrate they have a real physical illness. This is totally incorrect. As I mentioned above, fMRI has been used at length to study “hysteria”, and “conversion disorder” and the purpose has always been to show how “psychological” the condition really is. In my view, none of these studies is persuasive (lots of bad reverse inferencing, poor control groups and a selective discussion of “compatible” findings). But the point is, be very, very wary.
 
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Woolie

Senior Member
Messages
3,263
Jonathan Edwards said:
I would like to get back to the issue of types of belief because I think they are relevant to the friction point between patients and scientists and also to what seems clunky about Mark Edwards's approach.

"Relevant to the friction point????". The idea we are somehow supersensitive to terms that make us feel bad about ourselves:(, and this is our "friction point"? Sounds very Wessely and White, and a great way to silence patients.

Our "friction point" is seeing money go towards work that builds on assumptions that should have been thrown out long ago, and that don't lead to real effective treatment (just behavioural therapies and antidepressants). Oh, and serves to further delay research into real treatment.:grumpy:
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
There are indeed inhibitory fibers. Its not suspicion. I am speaking from 1995 neuroscience though, things change. It was integral to my neural model that you can have excitatory and inhibitory fibers. I think the visual cortex uses them. My science on this is waaaaayyyy out of date though.

Yes of course Alex. I might have said most or the majority of brain activity is inhibitory but that would be too strong. Perhaps I should have said that I suspect that brain activity is weighted towards inhibition.

BTW - I found that paper on near-death experiences I mentioned. I'm sure there are many holes in the 'dying brain' model as presented but an interesting discussion of 'life after death' which must of course represent an extreme case of cartesian dualism :

http://www.critical-thinking.org.uk/paranormal/near-death-experiences/the-dying-brain.php
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
The point of this is that at any instant there are far too many sensory inputs to think about so the system has to weed out the most salient until there is just one pattern that gets through to awareness.

I think it is not unreasonable to suggest that in ME this filtering process might be skewed. I doubt it is a purely quantitative thing. If you do not have inhibition at about the usual level you probably get seizures - everything starts exciting everything else. But collateral inhibition might fail in a more subtle way in nociceptive pathways.

Interesting in this context that one study found reduced latency and abnormally high responses to both target and non-target visual stimuli in a sub-group of young CFS patients :

Event-related potentials in Japanese childhood chronic fatigue syndrome.
Akemi Tomoda, Kei Miyuno, Nobuki Murayama, Takaka Joudoi, Tomohiko Igasaki. Journal of Pediatric Neurology, January 2007.

http://iospress.metapress.com/content/w14pg23t125337q8/
 

Jonathan Edwards

"Gibberish"
Messages
5,256
"Relevant to the friction point????". The idea we are somehow supersensitive to terms that make us feel bad about ourselves:(, and this is our "friction point"? Sounds very Wessely and White, and a great way to silence patients.

Our "friction point" is seeing money go towards work that builds on assumptions that should have been thrown out long ago, and that don't lead to real effective treatment (just behavioural therapies and antidepressants). Oh, and serves to further delay research into real treatment.:grumpy:

I think that is a little unfair Woolie. I might even suggest you are being supersensitive to my use of words! What I was implying by friction point is the point of very reasonable sensitivity on the part of patients to usage of 'belief' by people like Mark Edwards in a way that amounts to doublespeak. My impression is that Edwards would like to think that he is on the patients' side but he is never going to get there unless he is more rigorous about what his model really means. If 'belief' can include your hypothalamus believing that it needs to increase your heart rate on standing because it is being inappropriately stimulated by autoantibodies then nobody is going to mind but belief is not a very helpful term for that. If belief requires 'having been convinced' at some higher level involving social interaction and probably childhood trauma and needs to be unconvinced by CBT then red flags start waving big time.

I agree that we want research into real treatment but having sat around a table with the people who seem most interested in delivering that (Hornig, Fluge, Peterson, Marshall Gradisnik, Newton, Holgate, Baraniuk, Chia, Keller, Scheibenbogen, Blanco, Bergquist, take your pick) there is a consensus that trying to find some signal in the brain that shows what is being done to it by whatever is one of the most promising strategies, if not the most promising. I am leaning over backwards to give the benefit of the doubt at times, I agree, because I think models are muddled. However, I am more interested here in trying to analyse the general reasons for the muddling rather than get involved in specific instances.

I agree that the issue of different types of description is central. I guess that out points of view may differ in that I think the solution has to be to face up to the need to find a way of translating one into the other in physical dynamic terms - to be physicalist about it if you like. It is interesting to me that neuroscientists quote David Marr (who as you will know was undoubtedly one of the most gifted neuroscientists of all time but died in 1980 aged about 30) about levels of description. Marr claimed that there was a 'functional' level beyond the lower purely structural and dynamic levels that in principle could not be translated into the lower levels. I think he was wrong. It is a cop out. The translation may be intractable at present but that does not mean every effort should not be made to try and solve it. I think the psychological or experiential description has to be translatable into neurobiology. But that translation might serve to strengthen precisely the points that you are making - that inappropriate conclusions are being drawn from correlations on scans because people are making translations that are physically incoherent but pass muster because neuroscience is sloppy.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Marr claimed that there was a 'functional' level beyond the lower purely structural and dynamic levels that in principle could not be translated into the lower levels. I think he was wrong. It is a cop out.
I think you are right about that, and if you look into the research on artificial life you will see this sort of thing investigated, though for simplistic computational systems. I think it is in principle explicable, but its not always cheap, convenient or easy to understand. In translating between levels of description you might need to go back and forth, and every time you do that there is a chance you may misinterpret things, a chance for error. I would argue its hard to do reliably, but definitely not impossible. Indeed it is the grounding from one level to a lower one that makes it possible for claims at a higher level to be considered as scientifically sound. It comes down to mechanisms.

The problem with psychological mechanisms, though this varies with the branch of psychology (or psychiatry) is that its very hard to get the kind of low level brain detail we need. I am not sure the technology is really adequate yet. I think one day it might be. I think on that day psychology and neuroscience researchers will be like kids in a candy store, and may overstep the mark like we saw in genomics. Then, later, when the science clarifies a little, the chaff will get largely blown away and we will see the kernels of the things that are really important.

However it is the need for such technology that has the best chance of driving the development of such technology. I do not think it can be easily forced like in the human brain project. To quote an old saying (from the USA I think, I forget right now who said it) you railroad when its time to railroad. So many things have to come before you can build a rail network, and I think we tend to forget that.

PS: I think a similar problem occurs in symbolic logic. The translation to logic and the translation back to reality allows for serious error.
 

Hip

Senior Member
Messages
17,874
It worth mentioning that this friction between patients and doctors/researchers occurs not just in ME/CFS, but apparently also in other diseases that have been classified as functional disorders. Doctors tend to see functional disorders as having a psychological cause, whereas patients usually feel sure the cause is physical.

As we know, functional disorders include ME/CFS, fibromyalgia, irritable bowel syndrome, interstitial cystitis (which can be an awful disease in some cases), irritable bladder, lower back pain of unknown cause, non-cardiac chest pain.

The Wikipedia article on MUPS / medically unexplained physical symptoms (aka functional disorders) nicely summarizes the doctor–patient relationship in the case of these functional diseases:
The lack of known etiology in MUPS cases can lead to conflict between patient and health-care provider over the diagnosis and treatment of MUPS. Most physicians will consider that MUPS most probably have a psychological cause (even if the patient displays no evidence of psychological problems).

Many patients, on the other hand, reject the implication that their problems are "all in their head", and feel their symptoms have a physical cause. Diagnosis of MUPS is seldom a satisfactory situation for the patient, and can lead to an adversarial doctor-patient relationship. The situation may lead a patient to question the doctor's competence.

It seems the problem here is that most physicians and I presume much of the psychiatric profession assume by default that functional disorders have psychological causes.

This default position is rather illogical, because in no other area of medicine do you by default ascribe psychological causes to physical symptoms. OK, there may be no physical abnormalities detected in the functional disorder patient, but detection physical of abnormalities depends on the current state of medical technology. Thus there is no logical justification in assigning mental causes to physical symptoms just because you cannot observe any physical abnormalities.



Though in some respects, this default position of ascribing psychological causes is partly understandable, because the physical symptoms in functional disorders often come along with mental symptoms such anxiety, depression, fatigue and brain fog, which may make the average doctor then jump to the conclusion that both the physical and mental symptoms could both underpinned by psychological factors.

Here on PR we may hold a more enlightened view, and appreciate that both the physical and mental symptoms of a functional disorder are likely caused by something along the lines of autoantibodies affecting both the body and brain, or by a viral infection found both in bodily organs and the brain; but your average doctor sees the conjunction of physical and mental symptoms that appear in functional disorders, and sees no immediately obvious physical explanations in the body, and then 9 times out of 10, settles for a psychological rather than a physiological explanation.

It is in fact very unfortunate that functional disorders often come with mental symptoms; if that were not the case, then I don't think these disorders would have been viewed by so many doctors as having a psychological origin.



I also suspect that one significant — but rarely talked about — reason why doctors prefer to give a psychiatric diagnosis to patients with functional disorders is that it quickly gets the patient off their hands, out of their office, and into the care of a psychiatrist.

Outside of psychiatrists and psychologists, most human beings, including doctors, do not really like dealing with individuals exhibiting mental symptoms such a depression or anxiety. Any person with such mental symptoms will often make ordinary people feel uncomfortable, or worse still, annoyed and irritated. The average person, including the average doctor, is just not well equipped for dealing with people who have significant anxiety, depression or other psychiatric symptoms.

In fact my impression is that many GPs would be more comfortable looking at a wart on a patient's anus than dealing with depression or anxiety in a patient. This discomfort in dealing with mental symptoms in patients, including in functional disorder patients, may compound the problem of defaulting to a psychological explanation for functional disorders.



So if GPs are not comfortable with dealing with mental health, and psychiatrists have too much propensity to viewing even physical symptoms as having a psychological cause, what we need is a new breed of medical professional that is adept at dealing with a patient's mental symptoms, but also has the biochemical nous to be able to consider physical causes of physical symptoms — and even physical causes of mental symptoms.
 
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Woolie

Senior Member
Messages
3,263
I think that is a little unfair Woolie. I might even suggest you are being supersensitive to my use of words!

Yes, sorry, it was unfair. Especially since you are one of the few people that is really listening to us. I suppose the frustration of it all, seeing yet more research efforts going in what I think is the same old backwards direction. I'm also acutely aware of how patients' concerns have been silenced by casting them as somehow simply personally "uncomfortable" with a psychogenic interpretation.

And maybe I did only speak for myself - maybe some of us here on PR are worried about words like "belief"?

I think the psychological or experiential description has to be translatable into neurobiology

I think we really do agree on this. To me, this is the very reason we refer to these as "levels of description". But we're not there yet - if ever - and we need to be aware of the dangers of incorrect translation.

If 'belief' can include your hypothalamus believing that it needs to increase your heart rate on standing because it is being inappropriately stimulated by autoantibodies then nobody is going to mind but belief is not a very helpful term for that. If belief requires 'having been convinced' at some higher level involving social interaction and probably childhood trauma and needs to be unconvinced by CBT then red flags start waving big time.

If you're talking about the psychogenic movement disorder/Bayesian stuff, then Edwards talks about various levels of "belief". The patients form a powerful and very conscious belief that they have a movement disorder (when they in fact don't, or at least not any more), but this belief becomes a self-fulfilling prophecy because it operates to shape their movements at pre-conscious level. There's no role in the model for childhood trauma. But there needs to be psychopathology for the powerful belief to be formed/maintained: depression, anxiety, an intense focus on bodily symptoms (and/or too much time spent on forums like this one ;)).

If 'belief' can include your hypothalamus believing that it needs to increase your heart rate on standing because it is being inappropriately stimulated by autoantibodies then nobody is going to mind but belief is not a very helpful term for that

To cut through some of the terminological confusion, we could instead put the focus on causation. In your example, the question is: is the problem caused or significantly exacerbated by a maladaptive response from the hypothalamus? To the extent that changing its response could significantly improve the condition and/or its major symptoms (without intervening at the level of autoantibodies)?

Or is the hypothalamus responding normally and the root cause is the autoantibodies themselves? To the extent that only changing the latter will lead to real improvement?

My worry with the Edwards/Harrison thing is if they study the first type of question without looking at the second (which seems likely given what has been reported), they will end up with an incorrect causal model - a maladaptive brain response model - when the real problem is way further downstream.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
If input to, and output from, the hypothalamus is carrying aberrant signals from processes elsewhere, then the hypothalamus will be working overtime to fix things. Further, if blood supply to the hypothalamus is poor then it might not be working right either. Finally, I do not recall reading the exact description of acetylcholine M4 receptor distribution. That might affect the hypothalamus as well, either directly or via changes in the brain stem.
 

nandixon

Senior Member
Messages
1,092
Feyman actually goes into the phislosophers' lion's den in chapter 2.6. He makes the mistake of saying that measurements affect what is measured. Leibniz knew that this is flawed - causal statements of this sort go out of the window once we are talking fundamental reality.
Just to be clear, you're not saying that Feynman is wrong at the quantum level, are you?

Feynman is very likely correct where he states:
2. The Relation of Wave and Particle Viewpoints

2--6 Philosophical implications

.....It has always been known that making observations affects a phenomenon, but the point is that the effect cannot be disregarded or minimized or decreased arbitrarily by rearranging the apparatus.....
(emphasis added)

The Delft University experiment published just last week seems pretty close to making it a certainty now:

Loophole-free Bell inequality violation using electron spins separated by 1.3 kilometres

(There appears to be an additional experiment still to be done to try and close a final potential loophole, as noted in this layperson's summary of the study here:

Sorry, Einstein. Quantum Study Suggests ‘Spooky Action’ Is Real.)
 

Jonathan Edwards

"Gibberish"
Messages
5,256
I think you are right about that, and if you look into the research on artificial life you will see this sort of thing investigated, though for simplistic computational systems. I think it is in principle explicable, but its not always cheap, convenient or easy to understand. In translating between levels of description you might need to go back and forth, and every time you do that there is a chance you may misinterpret things, a chance for error. I would argue its hard to do reliably, but definitely not impossible. Indeed it is the grounding from one level to a lower one that makes it possible for claims at a higher level to be considered as scientifically sound. It comes down to mechanisms.

The problem with psychological mechanisms, though this varies with the branch of psychology (or psychiatry) is that its very hard to get the kind of low level brain detail we need. I am not sure the technology is really adequate yet. I think one day it might be. I think on that day psychology and neuroscience researchers will be like kids in a candy store, and may overstep the mark like we saw in genomics. Then, later, when the science clarifies a little, the chaff will get largely blown away and we will see the kernels of the things that are really important.

However it is the need for such technology that has the best chance of driving the development of such technology. I do not think it can be easily forced like in the human brain project. To quote an old saying (from the USA I think, I forget right now who said it) you railroad when its time to railroad. So many things have to come before you can build a rail network, and I think we tend to forget that.

PS: I think a similar problem occurs in symbolic logic. The translation to logic and the translation back to reality allows for serious error.

Sorry, I have got a bit behind with minds and brains thinking about PACE. I absolutely agree with all this post.