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What do you think of the work of Michael Maes?

MeSci

ME/CFS since 1995; activity level 6?
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I'm posing this question because another member commented in another thread that he did not trust his work.
 

Hip

Senior Member
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Can you post a link to that comment, so we can read what work this concerns.
 

alex3619

Senior Member
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13,810
Location
Logan, Queensland, Australia
Can you post a link to that comment, so we can read what work this concerns.
There was no work cited in that comment, just a general statement. However it was in response to my posting a comment on an earlier Maes paper showing high levels of autoantibodies in ME, though not specific autoantibodies. There is a thread on this somewhere.
 

Beyond

Juice Me Up, Scotty!!!
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I like the work of Maes a lot and not only in CFS but he hasn´t found a definite cause and therefore treatment yet. He abandoned the Leaky Gut thing a while ago because only a subset of CFS people cured or improved significantly with it (this subset of people was not surprisingly characterized by younger age and less time of disease)

For me, leaky gut is an important factor but is logical than in degenerative cases of years or decades other things have become limiting factors like HPA dysregulation. Plus things like Lyme and other chronic infections should be taken into account. The involved variables are many and it is unlikely to find a single cause for everyone, which is what researchers seems to be obsessed with. A more broad or "holistic" view is needed IMO.
 
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MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
I like the work of Maes a lot and not only in CFS but he hasn´t found a definite cause and therefore treatment yet. He abandoned the Leaky Gut thing a while ago because only a subset of CFS people cured or improved significantly with it (this subset of people was not surprisingly characterized by younger age and less time of disease)

For me, leaky gut is an important factor but is logical than in degenerative cases of years or decades other things have become limiting factors like HPA dysregulation. Plus things like Lyme and other chronic infections should be taken into account. The involved variables are many and it is unlikely to find a single cause for everyone, which is what researchers seems to be obsessed with. A more broad or "holistic" view is needed IMO.

According to this 2008 paper Maes found that over half of the patients improved significantly, some achieving remission, and I thought that all had some improvement but am not sure where I took that from. Right now I can't get my head round Table 2 - could someone do an Idiot's Guide?

This 2012 paper that Alex indirectly linked to indicates that Maes was still interested in issues that relate to leaky gut when conducting that study, as it refers to LPS (lipopolysaccharides) from enterobacteria.

I agree that it is unlikely that one thing is responsible for all cases of ME, but leaky gut could theoretically be at the basis of many - if not all - symptoms, by leading to the production of autoantibodies against a wide range of cells, including those on mitochondria and in the HPA axis. Which antibodies are produced may depend on genetic and environmental factors, i.e. what gets into an individual's bloodstream from the gut, and how the body responds. This could also explain the symptom changes that occur during the disease process.
 

Beyond

Juice Me Up, Scotty!!!
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Murcia, Spain
I meant that he has stopped trying to heal the leaky gut in more trials and that is telling. Well, I thought so, they have had 5 years now to try an improved approach. I somehow feel he and others didn´t conclude that the 2008 results were a definite success. They add at the end of the study that those that didn´t "heal" or even improve have limiting factors beyond leaky gut. In the paper it is said that 52% of patients improved or went into remission which means 48% did not improve.

From all my reading and experience I would say that when leaky gut is not te cause of chronic inflammatory autoimmune illnes it is a "causative consequence", an important chain in the disease cascade. Which means that a lot of people that I have known online with autoimmunity etc have discovered that they have leaky gut. For instance, everyone with Hashimoto´s Thyroiditis seems to have leaky gut, but not only that, intestinal permeability seems to be what decides if Chron´s disease patients in remission stay on remission or relapse. The etiologic nature of leaky gut in autoimmunity is pretty obvious but that is not to say all autoimmunity comes from it.

The work of Maes is in fact one of my favourites. In his last work he digs deeper in the inflammatory condition of depression. We need more researchers like him. Here you have a good list from google scholar: http://scholar.google.es/citations?...=1wzMZ7UAAAAJ&pagesize=100&view_op=list_works

For me is not in doubt if I need to heal my gut, but what limiting factors I need to deal with first or at the same time as healing it. Note that low adrenal hormones, low glutathione/methylation, or thyroid, or estrogen dominance etc can make impossible to maintain gut integrity despite of treating it directly.
 
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Instinctively sceptical, but largely from a position of ignorance.

I don't think it's likely to do much to harm patients, so haven't really dug in to any of it, but the little I have read has left me feeling uncomfortable (even if I can't remember exactly why now). I think Jonathan Edwards was critical of a paper that was passed to him too.

I'm being honest about my assumptions, rather than commenting because I think my views on this matter are of any real value at the moment.
 
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10,157
Biological underpinnings of the commonalities in depression, somatization, and Chronic Fatigue Syndrome.

Anderson G, Maes M, Berk M.

Med Hypotheses. 2012 Jun;78(6):752-6. Epub 2012 Mar 23.

Abstract
BACKGROUND:
Somatization is a multisomatoform disorder characterized by medically unexplained, functional or psychosomatic symptoms. Similar somatic symptoms are key components of depression and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

METHODS:
This paper reviews the evidence that such symptoms are organically based. We use the term "physio-somatic" to describe these symptoms.

RESULTS:
Inflammation, cell-mediated immune (CMI) activation and alterations in the tryptophan catabolite (TRYCAT) pathway are associated with the physio-somatic symptoms of depression, ME/CFS and/or somatization. Proinflammatory cytokines, decreased tryptophan and aberrations in TRYCATs may cause physio-somatic symptoms, such as fatigue, autonomic symptoms, hyperalgesia and somatic presentations.

CONCLUSIONS:
The data suggest co-ordinated and interacting biological pathways driving the occurrence of physio-somatic symptoms across these three disorders, giving a biologically validated "pathway phenotype". These data have far-reaching implications for DSM-IV diagnostic conceptualizations of somatization (and ME/CFS) suggesting the presence of an emerging organic explanation.

Future research should focus on the role of immune regulation, and co-ordination, of neuronal activity and, through larger data sets, ultimately creating new, biologically validated classification rules.

These data have implications for the development of novel therapies utilizing these insights, buttressing the role of psychotherapy in psychosomatic presentations. (my bold)

Well, I don't trust this at all. The last line - therapies? Why not treatments? Psychotherapy for ME to treat the biological underpinnings? . Puleez and really? Psychosomatic presentations? I am extra cranky today from extreme nausea so I better stop even though I could go on. Oh and just why the heck is he comparing ME to depression anyways? Why not compare it to MS, AIDs, Cancer? I know he has done other research that I haven't read but this is really awful.
 

Hip

Senior Member
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17,824
I thought the papers that Maes has published with Twisk expressing a very strong views against CBT/GET were great:

A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS

"We conclude that it is unethical to treat patients with ME/CFS with ineffective, non-evidence-based and potentially harmful "rehabilitation therapies", such as CBT/GET."


Chronic fatigue syndrome: la bête noire of the Belgian health care system
 

Hip

Senior Member
Messages
17,824
I also liked the papers he has published on how fixing leaky gut sometimes helps ME/CFS, and has even lead to full remission:

Normalization of the increased translocation of endotoxin from gram negative enterobacteria (leaky gut) is accompanied by a remission of chronic fatigue syndrome.

Normalization of leaky gut in chronic fatigue syndrome (CFS) is accompanied by a clinical improvement: effects of age, duration of illness and the translocation of LPS from gram-negative bacteria.

There is a thread on these papers:

Fixing Leaky Gut Helps ME/CFS, and Sometimes Achieves Full Remission

I found it particularly in interesting he theory that LPS (lipopolysaccharide) leaking from the gut ("LPS translocation") may underpin ME/CFS in some cases.

LPS is a potent inducer of the Th2 immune response (ref: here), and one of the most potent pro-inflammatory substances known to man. Given that ME/CFS is a disease in which patients are known to be stuck in the Th2 mode, it makes sense that fixing a possible leak of LPS from the gut may help some ME/CFS patients get back to the desired Th1 response, and then get remission from ME/CFS.

However, I suspect that not many ME/CFS patients actually have leaky gut, so then this leaking LPS etiology would not apply.

Nevertheless, it does indicate that factors like LPS, which shift you away from Th1 and over to Th2, may be involved in maintaining the disease state of ME/CFS. It is interesting that mold also shifts from Th1 to Th2.

Thus even if this leaky gut approach to treating ME/CFS has limited applicability, the wider ramifications of this study might be interpreted as a validation of the Th1 to Th2 shift model of ME/CFS. So for those seeking cures/treatments for ME/CFS, Maes work suggest that we should be looking for and addressing other pernicious factors (like mold) that shift from Th1 to Th2.
 
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MeSci

ME/CFS since 1995; activity level 6?
Messages
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Location
Cornwall, UK
Well, I don't trust this at all. The last line - therapies? Why not treatments? Psychotherapy for ME to treat the biological underpinnings? . Puleez and really? Psychosomatic presentations? I am extra cranky today from extreme nausea so I better stop even though I could go on. Oh and just why the heck is he comparing ME to depression anyways? Why not compare it to MS, AIDs, Cancer? I know he has done other research that I haven't read but this is really awful.

I can't figure out which camp he is standing in from this abstract. I do have a degree of brain fog, which isn't helping, but it's not clear to me whether he is talking about moving towards a biological explanation of illnesses considered to be mental, or not. The 'buttressing' and 'psychosomatic' references don't help my confusion! Could he have, or pretend to have, a foot in both camps in order to increase the chances of publication?
 

Beyond

Juice Me Up, Scotty!!!
Messages
1,122
Location
Murcia, Spain
From what I have read, Maes is a big proposer of the phyisiological side of what is labelled as "mental illness". See his work on depression and inflammatory markers or suicidality and elevated oxidative stress.

I want to add something interesting that gives a bit of vailidity to the psycho-babble crowd though, people getting stress do get more inflammatory cytokines in blood, mice that fail in fighting and become "losers that do not get laid" also express inflammatory genes and lastly adults that suffered abuse or trauma as kids get chronic illness more often.

So it is true that psychology has a role in disease but the belief that some illnesses are purely psychogenic is very damaging to patients as the physical factors are far more important.
 
Messages
10,157
I can't figure out which camp he is standing in from this abstract. I do have a degree of brain fog, which isn't helping, but it's not clear to me whether he is talking about moving towards a biological explanation of illnesses considered to be mental, or not. The 'buttressing' and 'psychosomatic' references don't help my confusion! Could he have, or pretend to have, a foot in both camps in order to increase the chances of publication?

I don't know what he's doing either. The title of the paper is enough to set my blood boiling -- Biological underpinnings of the commonalities in depression, somatization, and Chronic Fatigue Syndrome. I can't imagine a paper called 'Biological underpinnings of the commonalities in depression, somatization, and Multiple Sclerosis/Cancer/AIDs/Diabetes etc' with the offering of 'therapies' and the 'buttressing of the role of psychotherapy in psychosomatic presentations' of these diseases/illnesses. It's actually quite Wessely-like -- him saying, yes, there are organic things going on but you still need psychotheraputic interventions to rid yourself of ME. Tying ME to somatization which is an unproven psychiatric disorder akin to hysteria is ridiculous. Would you tie cancer, diabetes to somatization. I just can't trust somebody who further insults the ME community in this manner. If he wants to study biological underpinnings then he should leave the psychobabble out totally. Hope that all made sense.
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
From what I have read, Maes is a big proposer of the phyisiological side of what is labelled as "mental illness". See his work on depression and inflammatory markers or suicidality and elevated oxidative stress.

I want to add something interesting that gives a bit of vailidity to the psycho-babble crowd though, people getting stress do get more inflammatory cytokines in blood, mice that fail in fighting and become "losers that do not get laid" also express inflammatory genes and lastly adults that suffered abuse or trauma as kids get chronic illness more often.

So it is true that psychology has a role in disease but the belief that some illnesses are purely psychogenic is very damaging to patients as the physical factors are far more important.

I agree. There have been quite a few studies showing the effects of stress on the HPA axis, immune system and wound healing, for example. This paper talks mainly about the latter.

Everything we do and experience causes physiological changes.
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
I don't know what he's doing either. The title of the paper is enough to set my blood boiling -- Biological underpinnings of the commonalities in depression, somatization, and Chronic Fatigue Syndrome. I can't imagine a paper called 'Biological underpinnings of the commonalities in depression, somatization, and Multiple Sclerosis/Cancer/AIDs/Diabetes etc' with the offering of 'therapies' and the 'buttressing of the role of psychotherapy in psychosomatic presentations' of these diseases/illnesses. It's actually quite Wessely-like -- him saying, yes, there are organic things going on but you still need psychotheraputic interventions to rid yourself of ME. Tying ME to somatization which is an unproven psychiatric disorder akin to hysteria is ridiculous. Would you tie cancer, diabetes to somatization. I just can't trust somebody who further insults the ME community in this manner. If he wants to study biological underpinnings then he should leave the psychobabble out totally. Hope that all made sense.

Yes, I don't like the wording either. Maybe it was one of the other authors who wrote/oversaw the wording? It doesn't really sound like Maes to me.
 

Snow Leopard

Hibernating
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Maes is one of a minority of researchers who looks for biological underpinnings to mental disease.

The language of his papers is the usual over-hyped or stuff of exaggerated importance that is common in scientific research.

He seems to be taking a sort of scatter-gun approach to research, being involved with many things, hoping that something sticks.

I think he has a reputation of doing something different to the rest of the field, which was at least good enough to get a visiting scholar position in Australia.
 
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10,157
Yes, I don't like the wording either. Maybe it was one of the other authors who wrote/oversaw the wording? It doesn't really sound like Maes to me.

His name is on the paper so he must agree with what was written. I honestly don't know how much he had to do with the actual writing of it but this is his work. What is wrong with the following statement? (comes from the conclusion in the paper).

These findings have far-reaching consequences. (a) Functional "somatic" symptoms, classically explained by psychological factors, appear to have a biological substrate. (b) This challenges current DSM-IV diagnostic criteria for somatization, depression, and ME/CFS, and suggests revision, based on the incorporation of biological markers.

I am just hazarding a guess that as soon as the IOM is finished with ME that it will actually show up in the next edition of DSM but that's totally another subject.