so whats go to come from the NIH meeting??

[usedtobeperkytina]

It's all about the biomarkers folks. Whether together as one or in subgroups, we have to have biomarkers to get research. Sad fact, but true. So, if we have some subgroups of us with these biomarkers, subgroups with other biomarkers, then it can be used in research now.

The paper could be Patients who meet the CCC and Fukuda who have NK Cell dysfunction of ____ % showed 66% improvement with ______.

It can be done now, without changing labels.

Tina

 

[anciendaze]

It's all about the biomarkers folks. Whether together as one or in subgroups, we have to have biomarkers to get research. Sad fact, but true. So, if we have some subgroups of us with these biomarkers, subgroups with other biomarkers, then it can be used in research now.

The paper could be Patients who meet the CCC and Fukuda who have NK Cell dysfunction of ____ % showed 66% improvement with ______.

It can be done now, without changing labels.

The catch with biomarkers is that you aren't going to get one that matches a diagnostic category if that category is a social construct rather than a biological entity. At this point, I feel certain suggested biomarkers will cause ME/CFS to overlap other diagnostic categories. This will result in another round of battles over definition, (and you know what kinds of definitions are out there waiting.) In the meantime, we will be stuck with the "ill-defined disease" label which has hamstrung research. (Strangely, this criticism never applies to any "real" existing disease categories which ME/CFS overlaps, like MS.) This leads to a lack of funding, because "the science just isn't there".

 

[usedtobeperkytina]

And that's why I am saying that you can keep the social construct label if you want (talking to any one in government or those who created it), but make it more defined in studies as to what biological abnormality is seen in the patients you are studying. There is enough of us.

I guess what I am saying is that there may not be just one biomarker. But, there are biomarkers that can be used for subgroups, even a majority of us. So journals and government agencies like biomarkers. Give them one. Stop trying to prove there are biomarkers for the whole group. Prove that those in the group with a certain biomarker also have _______________________ or respond to __________________________. Peterson said that low NK function was the closest thing he knew of to use as a biomarker. So, let's use it. I know it may not apply to all of us. But using it will move the science forward for all of us.

We seem to always be defending and trying to prove that for which we already have proved. Low natural killer cell function has been shown in majority of us since 1987. So use it. As you said, they created a catch all. It may not be we all have the same thing. And even if we do, the biomarker may subside, just as our symptoms do. Mary said that happened to her. This is no different from cancer. But let's use what we have to get published and get more research funding.

Well, just my 2 cents worth.

Tina

 

[heapsreal]

And that's why I am saying that you can keep the social construct label if you want (talking to any one in government or those who created it), but make it more defined in studies as to what biological abnormality is seen in the patients you are studying. There is enough of us.

I guess what I am saying is that there may not be just one biomarker. But, there are biomarkers that can be used for subgroups, even a majority of us. So journals and government agencies like biomarkers. Give them one. Stop trying to prove there are biomarkers for the whole group. Prove that those in the group with a certain biomarker also have _______________________ or respond to __________________________. Peterson said that low NK function was the closest thing he knew of to use as a biomarker. So, let's use it. I know it may not apply to all of us. But using it will move the science forward for all of us.

We seem to always be defending and trying to prove that for which we already have proved. Low natural killer cell function has been shown in majority of us since 1987. So use it. As you said, they created a catch all. It may not be we all have the same thing. And even if we do, the biomarker may subside, just as our symptoms do. Mary said that happened to her. This is no different from cancer. But let's use what we have to get published and get more research funding.

Well, just my 2 cents worth.

Tina

TOTALLY AGREE< AMEN!!!!

 

[WillowJ]

hear, hear!

 

[insearchof]

What would make NKC a distinctive bio marker in CFS?

Brain dead right now, so excuse this question if it has been address already - but NK abnormalities are not restricted to CFS patients.

Therefore, why is NKC activity being promoted as a bio marker for CFS?

Is there something distinctive in NKC activity in CFS that distinguishes it from other illnesses that also show poor NKC activity or abnormality?

Or is it, NKC activity plus another bio marker? If so, are they distinctive enough to set a sub set of CFS patients apart from other illnesses?

 

[heapsreal]

Brain dead right now, so excuse this question if it has been address already - but NK abnormalities are not restricted to CFS patients.

Therefore, why is NKC activity being promoted as a bio marker for CFS?

Is there something distinctive in NKC activity in CFS that distinguishes it from other illnesses that also show poor NKC activity or abnormality?

Or is it, NKC activity plus another bio marker? If so, are they distinctive enough to set a sub set of CFS patients apart from other illnesses?

I agree its not restricted to cfs but its common abnormality found in cfs and it also is proof for those doctors that say that cfs is a form of depression. Shouldnt also be used in isolation but maybe with other tests and symptoms. Its also may explain some co=infections in cfs as well.

cheers!!!

 

[usedtobeperkytina]

Well, either or.

If they can do a study just on CFS symptoms, making claims about one disease, then they can do a study on people with CFS and low Natural Killer Cells as a subgroup of that disease. I guess trying to say we all have one biomarker, considering the construct, may not ever work. How about we move past trying to prove a biomarker and use the one we have to say, "these folks with this disease who have this biological abnormality show this." It moves it to the next level. For example, how many with CFS who have low NK Cell function also have high level EBV titers?

So instead of getting a biomarker for all those in the arbitrarily-created "CFS" or even change the criteria (which is needed, just knowing that will take time), we can do studies now that use the biological abnormalities for groups within the CFS crowd and show what is happening or what can help them. Researchers can stop waiting for someone to fix Fukuda or subgroup it, just use it and create your own subgroups with biological abnormality for that group. The editor for the brain journal that was at the SoK meeting said he would be happy to include such details as a supplement.

One of the calls in the meeting were clinical trials. Why not a study of what treatments help CFS patients who have low natural killer cell function. If this could be validated, then physicians, whose focus is on treatment, will first diagnose CFS, then run a NK function test. If it comes back low, aha, he has something he can give that person.

To do this, move the science forward, we don't have to have to use a separate, distinctive biomarker which may not be coming because of the problems in defining who has it. But we can use the biological abnormalities we already have to subgroup and more clearly define the cohort for a study. No need to wait for someone else to do it. It can be done in studies now.

Tina

 

[Nielk]

`The best possible outcome of the meeting in my opinion

1-more funding for studies
2- more awareness of this being a real disease that warrants studying.
3- some of these experts pooling their expertise and work together to try to come up with a combined consensus as to how to proceed from here
4- more advocacy for our cause
5- Disseminate all this information to the medical profession at large throughout the country.

I watched the meeting on and off and what struck me at first was - wow, all these doctors/Biologists/professionals are seriously discussing our illness and trying to explain how they view it. I think that's a major victory for us. Even though they mostly had a different point of view-depending on what is their expertise, I hope they listened to what everyone had to say.
I hope they were genuinely interested to learn and not just there with tunnel vision as to their own viewpoint.

I wish they had discussed a name change.
I wish the patients that spoke up were more composed - (although I understand their utter frustration) - I feel that their words would have had more impact, if they weren't visibly so emotional.
I wish Dr. Mikovitz was more polished.

 

[floydguy]

And that's why I am saying that you can keep the social construct label if you want (talking to any one in government or those who created it), but make it more defined in studies as to what biological abnormality is seen in the patients you are studying. There is enough of us.

I guess what I am saying is that there may not be just one biomarker. But, there are biomarkers that can be used for subgroups, even a majority of us. So journals and government agencies like biomarkers. Give them one. Stop trying to prove there are biomarkers for the whole group. Prove that those in the group with a certain biomarker also have _______________________ or respond to __________________________. Peterson said that low NK function was the closest thing he knew of to use as a biomarker. So, let's use it. I know it may not apply to all of us. But using it will move the science forward for all of us.

We seem to always be defending and trying to prove that for which we already have proved. Low natural killer cell function has been shown in majority of us since 1987. So use it. As you said, they created a catch all. It may not be we all have the same thing. And even if we do, the biomarker may subside, just as our symptoms do. Mary said that happened to her. This is no different from cancer. But let's use what we have to get published and get more research funding.

Well, just my 2 cents worth.

Tina

I agree too. Let's start here. We must have something that starts to define us with proven objective tests. It may not be perfect at first but anything is better than vague references to fatigue and malaise. I happen to have low NK function but I don't care if there is a biomarker that I don't have as long as it is an accepted test and it differentiates us from anything that be construed as psychosomatic, MDD, etc.

 

[Snow Leopard]

it also is proof for those doctors that say that cfs is a form of depression. Shouldnt also be used in isolation but maybe with other tests and symptoms.

It is a problem that low NKC activity has also been inplicated in major depression...

 

[usedtobeperkytina]

unless

Unless, of course, these people diagnosed with depression actually have ME/CFS. And I know there are many in that situation.

Tina

 

[heapsreal]

Unless, of course, these people diagnosed with depression actually have ME/CFS. And I know there are many in that situation.

Tina

Thinking the same thing, how many people with depression/dysthymic disorder which is low energy depression are probably me/cfs too.

cheers!!!

 

[In Vitro Infidelium]

It is a problem that low NKC activity has also been inplicated in major depression...

Unless, of course, these people diagnosed with depression actually have ME/CFS.

High levels of misdiagnosis of CFS as depression is inevitable given the usual range of diagnostic bias found in primary care. There is another issue though, and that is the possibility that depression is a biochemical condition that may be precipitated by insult to the immune system - this is not an attractive notion to many M.E/CFS sufferers because it suggests an equivalence between depression and M.E/CFS, however once one detaches 'depression' from the Freudian and Jungian paradigms it has to be allowed that depression, like M.E/CFS is an illness of biochemical processes. From that perspective common NKC characteristics in 'major depression' and M.E/CFS isn't the problem that SL suggests, rather it may be a route to better description of the biochemical 'lansdcape' of a range of ill health within which both major depression and M.E/CFS happen to exist.

The idea of a perfect case description, which if it were apllied to all research inclusion criteria would allow revellation the unique biochemical processes of M.E/CFS is hopeless myth making. At this stage there is simply no evidence to suggest any specificity of underlying processes for a patient group (17 million CFS ? - 4 million 'Hyde' M.E ?) and it is highly probable that across the group multiple commonalities with other illness other illness processes exist. Understanding the interplay of the relevant processes as a whole, rather than looking for single 'unique' fingerprints, may well offer the most effective route to explaining of what actually makes M.E/CFS sufferers unwell. That the disease processes of M.E/CFS may include commonalities with biochemically mediated mental ill health should not be a concern.

IVI

 

[heapsreal]

High levels of misdiagnosis of CFS as depression is inevitable given the usual range of diagnostic bias found in primary care. There is another issue though, and that is the possibility that depression is a biochemical condition that may be precipitated by insult to the immune system - this is not an attractive notion to many M.E/CFS sufferers because it suggests an equivalence between depression and M.E/CFS, however once one detaches 'depression' from the Freudian and Jungian paradigms it has to be allowed that depression, like M.E/CFS is an illness of biochemical processes. From that perspective common NKC characteristics in 'major depression' and M.E/CFS isn't the problem that SL suggests, rather it may be a route to better description of the biochemical 'lansdcape' of a range of ill health within which both major depression and M.E/CFS happen to exist.

The idea of a perfect case description, which if it were apllied to all research inclusion criteria would allow revellation the unique biochemical processes of M.E/CFS is hopeless myth making. At this stage there is simply no evidence to suggest any specificity of underlying processes for a patient group (17 million CFS ? - 4 million 'Hyde' M.E ?) and it is highly probable that across the group multiple commonalities with other illness other illness processes exist. Understanding the interplay of the relevant processes as a whole, rather than looking for single 'unique' fingerprints, may well offer the most effective route to explaining of what actually makes M.E/CFS sufferers unwell. That the disease processes of M.E/CFS may include commonalities with biochemically mediated mental ill health should not be a concern.

IVI

I suppose this is where they need to marry up a few different diagnostic observation that differ between cfs and depression like PEM which happens with cfs and cortisol increases as well as endorphin release from exercise in depression, this doesnt seem to occur in cfs and we are talking mild exertion not full on training intensity. It all sounds very interesting but i think the main thing in cfs is immune dysfunction/abnormalities although the actual dysfunction could be different amongst other cfsers.

cheers!!!

 

[Camilla]

I watched the meeting on and off and what struck me at first was - wow, all these doctors/Biologists/professionals are seriously discussing our illness and trying to explain how they view it. I think that's a major victory for us. Even though they mostly had a different point of view-depending on what is their expertise, I hope they listened to what everyone had to say.
I hope they were genuinely interested to learn and not just there with tunnel vision as to their own viewpoint.

I wish they had discussed a name change.
I wish the patients that spoke up were more composed - (although I understand their utter frustration) - I feel that their words would have had more impact, if they weren't visibly so emotional.
I wish Dr. Mikovitz was more polished.

I completely agree, especially with the last two sentences. We need composed and professional advocates, both patients and researchers. I too fully understand the frustration of the patients (and share it 100%), but it is so important when we get a chance like this, to use it in an optimal way to get our message through. (And to show that we're NOT depressed.)

 

[In Vitro Infidelium]

I suppose this is where they need to marry up a few different diagnostic observation that differ between cfs and depression like PEM which happens with cfs and cortisol increases as well as endorphin release from exercise in depression, this doesnt seem to occur in cfs and we are talking mild exertion not full on training intensity. It all sounds very interesting but i think the main thing in cfs is immune dysfunction/abnormalities although the actual dysfunction could be different amongst other cfsers.

Differentiation is important, but we have to be prepared for an outcome that shows underlying biochemistry that is common (in part or in whole) to both M.E/CFS and to psychiatric illnesses, which is causative of M.E/CFS or in some way mediates the symptoms of M.E/CFS. At this stage in terms of research biochemical investigation is what should lead differentiation, with symptom based diagnostic criteria being used for comparitive grouping. Of course this raises many anxieties about conflation with 'depression', but unless we are to argue for M.E/CFS not being a 'neurological condition' then absolute distinction from psychiatric illness is not going to be possible in the process of research. For instance the occurrence of PEM and variable hormone release maybe genetically modulated responses to a common insult, which differentiates individuals into groups that on one side are characterised by major depression - acute or chronic, and on the other by chronic malaise.

IVI

 

[Snow Leopard]

Differentiation is important, but we have to be prepared for an outcome that shows underlying biochemistry that is common (in part or in whole) to both M.E/CFS and to psychiatric illnesses, which is causative of M.E/CFS or in some way mediates the symptoms of M.E/CFS.

Sure. Unless you buy into the dualistic approach, there will be biochemical pathways in common with psychiatric illness, for every disease from cancer to Amyotrophic lateral sclerosis. This is not the same as saying these pathways are of primary importance.

For instance the occurrence PEM and variable hormone release maybe gentically modulated responses to a common insult, which differentiate individuals into groups that on one side are characterised by major depression - acute or chronic, and on the other by chronic malaise.

That has been the working hypothesis of many "mainstream" CFS researchers over almost 25 years. It has borne no fruit. Perhaps because it isn't such a useful hypothesis, or perhaps this is due to the chronic underfunding of medical research for this disease.

By the way, merely stating that stress is a risk factor is unfalsifiable and not useful scientifically. However looking at biochemical stress responses in a compehensive longitudinal manner is a little more useful.

Now cortisol measures have been shown to reflect anticipated stressors during the day and therefore reflect activity levels to a degree. The literature shows that healthy individuals have significantly lower cortisol response on days of rest, particularly on the weekend as compared with workdays.
MDD/Anxiety, is associated with high UFC and waking salivary cortisol compared to healthy individuals, when both tested on workdays and so this finding can be considered specific and potentially useful.

Comparing CFS/ME patients to healthy individuals on workdays however is not such a bright idea and reflects poor study design. This is because most CFS/ME patients are not working and have generally uneventful days and so the low cortisol findings are nonspecific. This suggests that while stressors could have been part of an initial trigger, it is not a perpetuating factor in most patients. There may also be a subset of CFS/ME patients with Addison's disease like pathology and so this may dilute such findings.

One may however suggest that low activity is a perpetuating factor, the idea that such activity will stimulate the body back into a normal equilibirum. This seems to be the working hypothesis of many psychiatrists, but strangely the results on self-report questionaires in RCTs are usually not replicated in objective measures of activity. Nor are the improvements quite so impressive in a clinical setting (see the Belgian combined CBT/GET n=593 study - activity levels did not change and less patients were working at the 6 month followup, compared to baseline). The CBT results also seem to disappear in 5 year followups, unless the patient continued to recieve treatment (and still didn't lead to a cure for those patients).

But there is plenty of evidence on the contrary to the activity hypothesis. Merely increasing activity, without CBT style cognitive conditioning doesn't seem to help. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC555551/
A more sophisticated approach by Jason et al. found that activity increases can be beneficial, provided one remains within ones "energy envelope". http://www.ncbi.nlm.nih.gov/pubmed/18578185

But those improvements are only significant for a minority and it isn't likely to be (near) curative either.