@Valentijn before you jump into wrong conclusions, read first what the Wiki link states
Are endogenous depression and cfs close relatives?
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@Richie yes, there has been a controversy about it, but I believe (as does the Prof. at the CFS clinic who did the testing) that it is reliable. My urinary NT are btw also very low
Neurotransmitters excreted in the urin... [Neurosci Biobehav Rev. 2011] - PubMed - NCBI
Full document: http://www.surescreen.com/lifescienc...er_testing.pdf
https://www.neurorelief.com/index.ph...id=412&pid=149
http://www.corepsych.com/wp-content/.../08/kahane.pdf
Neurotransmitters excreted in the urin... [Neurosci Biobehav Rev. 2011] - PubMed - NCBI
Full document: http://www.surescreen.com/lifescienc...er_testing.pdf
https://www.neurorelief.com/index.ph...id=412&pid=149
http://www.corepsych.com/wp-content/.../08/kahane.pdf
I can't see the points you are making here proven in science. I have test of TH1/TH2 and no symptom of depression. You are guessing that TH1 causes low dopamine in PWCFS and therefore depression. My serotonin levels were normal. You don't have a dopamine test.
You take a theory. That's fine but it is just a theory. Maybe it is the right one for you.
When I was sold antidepressants in the 80's it was explained to me that they were developed as an immune system treatment initially and then only applied to depression when a higher mood was found. There are doctors who still believe that antidepressants work for an immune modulating effect. It's going to be individual.
Some doctors will just humour CFS patients into taking antidepressants because they believe it is purely a psychiatric disease. They would listen to your theory and write a prescription as quickly as possible nodding their heads and smiling.
Some doctors on the other hand would not accept the scenario you suggested. There is no proof that what you are saying is actually happening. A TH1/2 test isn't proof of your theory because there are PWCFS with these tests and no depression. There are PWCFS with high serotonin and normal levels. Antidepressants even in small quantities made me much worse.
Unless we have physical proof that CFS or ME and depression are related then it doesn't benefit us to link them.
If you benefit from antidepressents it not been hard in my experience to find a doctor to prescribe them. Whether you concede anything or not isn't important because you don't know what it is doing to you (i.e. you have no tests or proof).
You take a theory. That's fine but it is just a theory. Maybe it is the right one for you.
When I was sold antidepressants in the 80's it was explained to me that they were developed as an immune system treatment initially and then only applied to depression when a higher mood was found. There are doctors who still believe that antidepressants work for an immune modulating effect. It's going to be individual.
Some doctors will just humour CFS patients into taking antidepressants because they believe it is purely a psychiatric disease. They would listen to your theory and write a prescription as quickly as possible nodding their heads and smiling.
Some doctors on the other hand would not accept the scenario you suggested. There is no proof that what you are saying is actually happening. A TH1/2 test isn't proof of your theory because there are PWCFS with these tests and no depression. There are PWCFS with high serotonin and normal levels. Antidepressants even in small quantities made me much worse.
Unless we have physical proof that CFS or ME and depression are related then it doesn't benefit us to link them.
If you benefit from antidepressents it not been hard in my experience to find a doctor to prescribe them. Whether you concede anything or not isn't important because you don't know what it is doing to you (i.e. you have no tests or proof).
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Dan
I have had much on the list of symptoms you note.
PEM (immediate neuromuscular fatigue, generalised several day fatigue), OI, mild ataxia, not gastro paresis but gut stasis, coldt intolerance, sore throat, tender lymph nodes and more of my own etc.Fluctuationsa nd variations over 30 years.
I was undiagnosed for 13 years of 30. I did the "do it even though it will backfire thing" for most of these 13 years. I had to or I would have killed myself as the Drs would do 000000. for me. i do the same now, when I can, as I want a life. R. But I have also had some endogenous depression. Would you forbid me from asking whther there is a link? Would you say "Oh, well it's all been depression then?"
I have had a severely serotonin depleted system (if urinary evidence is reliable and I think in my case it is)..
I suspect the serotonin depletion is related in my case to TH1 activation of pathways away from serotoiinin production and towards neurotoxins also found in my urine. This is imo likely to be part of the organic illness , causing some depression and contributing to sleep difficulties.
In my case I believe there is an organic overlap between my CFS and serotonin depletion and conssequent depressive features, sleep problems etc.
Possibly the serotonin depletion is entirlely incidental, possibly. I doubt it.
Possibly I have Lyme or any other TH1 activating condition, possibly fibromyalgia, but I am symptom wise taken over 30 years, as well as having had several of the test abnormalities others on this board have, well within CFS/ME.
I have had much on the list of symptoms you note.
PEM (immediate neuromuscular fatigue, generalised several day fatigue), OI, mild ataxia, not gastro paresis but gut stasis, coldt intolerance, sore throat, tender lymph nodes and more of my own etc.Fluctuationsa nd variations over 30 years.
I was undiagnosed for 13 years of 30. I did the "do it even though it will backfire thing" for most of these 13 years. I had to or I would have killed myself as the Drs would do 000000. for me. i do the same now, when I can, as I want a life. R. But I have also had some endogenous depression. Would you forbid me from asking whther there is a link? Would you say "Oh, well it's all been depression then?"
I have had a severely serotonin depleted system (if urinary evidence is reliable and I think in my case it is)..
I suspect the serotonin depletion is related in my case to TH1 activation of pathways away from serotoiinin production and towards neurotoxins also found in my urine. This is imo likely to be part of the organic illness , causing some depression and contributing to sleep difficulties.
In my case I believe there is an organic overlap between my CFS and serotonin depletion and conssequent depressive features, sleep problems etc.
Possibly the serotonin depletion is entirlely incidental, possibly. I doubt it.
Possibly I have Lyme or any other TH1 activating condition, possibly fibromyalgia, but I am symptom wise taken over 30 years, as well as having had several of the test abnormalities others on this board have, well within CFS/ME.
CFS and depression could be both neuroinflammatory diseases in some or many cases. Both CFS and depression are just labels for a bunch of symptoms and not well defined diseases. By depression I mean the disease depression, not people reacting to adverse life circumstances with sadness, despair and grieving (which is what many people seem to think of when talking about depression).
Maybe the point I'm making here is that CFS and depression are not well defined entities, which can easily lead to misunderstanding. To communicate without misunderstanding we have to at least be sure to be talking about the same things.
Maybe the point I'm making here is that CFS and depression are not well defined entities, which can easily lead to misunderstanding. To communicate without misunderstanding we have to at least be sure to be talking about the same things.
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That you had it does not mean others should have it too.
My dopamine was very low. My reaction to antidepresants highly erratic. This and the serotonin may have been related to long term over stimulation by excitotoxins (quinolinate common in infection) or TNF Alpha. There may only a degree of correspondence between THi activatuion, tryptophan diversion tand serotonin depletion, but it is a reasonable theory. So why not discuss reasonable theories? Half the activity on this board is based on this.
The further problem is that there is not necessarily a direct correspondence between serotonin levels and depression.
I take your points on uncertainty, but you don't really answer my point, that I can defend myself from the idea that I am really just depressed by saying tot he doctor "well, my symptoms are mostly CFS, have been for years I have some reactive and immune activation can cause endogenous depression, so is my case likely to be psychogenic depression, uncomplicated endogenous depression, or is sth else going on, which might involve you considering I could have an undiagniosed illness, an infection, autoimmune etc so yoi do not just write me off as "depressed in denial"" That to me is practically useful. Sorry for he long sentence.
(When you go into it, you're right it is theory. Who knows maybe the broader scenario in some people is immune Th1 activation, excitotoxicty, HIGH short term dopamine/serotonin, followed by neuronal exhaustion, low serotonin/dopamine and in the case of resolved infection low/no quinolinate, but a fried brain. Symptoms of a fried brain........??...???)
The further problem is that there is not necessarily a direct correspondence between serotonin levels and depression.
I take your points on uncertainty, but you don't really answer my point, that I can defend myself from the idea that I am really just depressed by saying tot he doctor "well, my symptoms are mostly CFS, have been for years I have some reactive and immune activation can cause endogenous depression, so is my case likely to be psychogenic depression, uncomplicated endogenous depression, or is sth else going on, which might involve you considering I could have an undiagniosed illness, an infection, autoimmune etc so yoi do not just write me off as "depressed in denial"" That to me is practically useful. Sorry for he long sentence.
(When you go into it, you're right it is theory. Who knows maybe the broader scenario in some people is immune Th1 activation, excitotoxicty, HIGH short term dopamine/serotonin, followed by neuronal exhaustion, low serotonin/dopamine and in the case of resolved infection low/no quinolinate, but a fried brain. Symptoms of a fried brain........??...???)
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I agree
A further problem is that the seriousness of depression as a threat to life does not depend on whter or not it is reactive or endogenous (in as far as these are separable). People can lve with long term endogenous depression with no threat of suicide, while others will killl themselves over loss of a job, a partner etc. They are all clinical depressions and in that sense diseases.
What interests me is whether organic pathways in CFS/ME conssitent cases such as my own, may also have contributed to depression thru e.g. immune inflammation.I see nothing taboo at all in that, but as you point out, some depression is clearly more psychogenic and we are all defending ourselves against psychogenic theories of ME/CFS.
A further problem is that the seriousness of depression as a threat to life does not depend on whter or not it is reactive or endogenous (in as far as these are separable). People can lve with long term endogenous depression with no threat of suicide, while others will killl themselves over loss of a job, a partner etc. They are all clinical depressions and in that sense diseases.
What interests me is whether organic pathways in CFS/ME conssitent cases such as my own, may also have contributed to depression thru e.g. immune inflammation.I see nothing taboo at all in that, but as you point out, some depression is clearly more psychogenic and we are all defending ourselves against psychogenic theories of ME/CFS.
But when you build theories around findings (like TH1 or serotonin) and other CFS patients have the same tests and don't have depression then your theory isn't proven.
You may well be unlucky enough to have separate depression plus CFS in the same way people could have ME plus CFS or RA plus CFS.
All of these diseases may end up overlapping or have the same root cause but we don't know enough yet.
You may well be unlucky enough to have separate depression plus CFS in the same way people could have ME plus CFS or RA plus CFS.
All of these diseases may end up overlapping or have the same root cause but we don't know enough yet.
I'd expect symptoms to show some similarities if the same pathways were involved.
And there has been a LOT of research comparing depression and CFS. If there was some underlying organic similarity, it's very likely that they would have found it. Especially since the researchers were very invested in the "depressed psychiatry-bigots in denial" theory at the time.
And there has been a LOT of research comparing depression and CFS. If there was some underlying organic similarity, it's very likely that they would have found it. Especially since the researchers were very invested in the "depressed psychiatry-bigots in denial" theory at the time.
I tracked down the papers you were talking about, authored by Lucinda Scott.
http://www.ncbi.nlm.nih.gov/pubmed/10451910
The above study was unfortunately not properly gender matched (I would have done separate women or men comparisons as this was a common confounder of results back in 1999) and all subjects had already been selected due to having a reduced cortisol response to ACTH however the 'selected' nature of the participants is noted in the abstract and discussion.
I searched the citing articles on Google Scholar and no one seems to have published an attempted replication.
They hypothesised in the following paper that:
http://www.ncbi.nlm.nih.gov/pubmed/10403156
This was disproved in a later study by Lucinda Scott:
http://www.ncbi.nlm.nih.gov/pubmed/11104854
If the adrenal gland was atrophied, it would be expected that both DHEA and cortisol levels would be diminished. But it was found the DHEA levels were slightly higher (no statistical difference) at all time points before and after the ACTH stimulation test, but the cortisol response was diminished.
http://www.ncbi.nlm.nih.gov/pubmed/10451910
The above study was unfortunately not properly gender matched (I would have done separate women or men comparisons as this was a common confounder of results back in 1999) and all subjects had already been selected due to having a reduced cortisol response to ACTH however the 'selected' nature of the participants is noted in the abstract and discussion.
I searched the citing articles on Google Scholar and no one seems to have published an attempted replication.
They hypothesised in the following paper that:
http://www.ncbi.nlm.nih.gov/pubmed/10403156
This was disproved in a later study by Lucinda Scott:
http://www.ncbi.nlm.nih.gov/pubmed/11104854
If the adrenal gland was atrophied, it would be expected that both DHEA and cortisol levels would be diminished. But it was found the DHEA levels were slightly higher (no statistical difference) at all time points before and after the ACTH stimulation test, but the cortisol response was diminished.
Again, a serotonin (or receptor activity) deficiency hasn't been noted in CFS, in fact quite the opposite.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2127129/ "Increased brain serotonin function in men with chronic fatigue syndrome" Sharpe et al.
http://www.ncbi.nlm.nih.gov/pubmed/8938208 "Increased prolactin response to buspirone in chronic fatigue syndrome."
http://www.ncbi.nlm.nih.gov/pubmed/8550954 "Contrasting neuroendocrine responses in depression and chronic fatigue syndrome." Cleare, Wessley et al.
http://www.ncbi.nlm.nih.gov/pubmed/9226729 "Blunted serotonin-mediated activation of the hypothalamic-pituitary-adrenal axis in chronic fatigue syndrome."
http://www.ncbi.nlm.nih.gov/pubmed/1586780 "Possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome."
http://www.ncbi.nlm.nih.gov/pubmed/11352361 "Decreased tryptophan availability but normal post-synaptic 5-HT2c receptor sensitivity in chronic fatigue syndrome."
http://www.ncbi.nlm.nih.gov/pubmed/1282370 "Plasma and cerebrospinal fluid monoamine metabolism in patients with chronic fatigue syndrome: preliminary findings." Demitrack et al
Lastly, the lack of efficacy of SSRIs for depression (or anything else) in CFS patients suggests something else is at play.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(96)91345-8/abstract "Randomised, double-blind, placebo-controlled study of fluoxetine in chronic fatigue syndrome"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2127129/ "Increased brain serotonin function in men with chronic fatigue syndrome" Sharpe et al.
http://www.ncbi.nlm.nih.gov/pubmed/8938208 "Increased prolactin response to buspirone in chronic fatigue syndrome."
http://www.ncbi.nlm.nih.gov/pubmed/8550954 "Contrasting neuroendocrine responses in depression and chronic fatigue syndrome." Cleare, Wessley et al.
http://www.ncbi.nlm.nih.gov/pubmed/9226729 "Blunted serotonin-mediated activation of the hypothalamic-pituitary-adrenal axis in chronic fatigue syndrome."
http://www.ncbi.nlm.nih.gov/pubmed/1586780 "Possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome."
http://www.ncbi.nlm.nih.gov/pubmed/11352361 "Decreased tryptophan availability but normal post-synaptic 5-HT2c receptor sensitivity in chronic fatigue syndrome."
http://www.ncbi.nlm.nih.gov/pubmed/1282370 "Plasma and cerebrospinal fluid monoamine metabolism in patients with chronic fatigue syndrome: preliminary findings." Demitrack et al
Lastly, the lack of efficacy of SSRIs for depression (or anything else) in CFS patients suggests something else is at play.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(96)91345-8/abstract "Randomised, double-blind, placebo-controlled study of fluoxetine in chronic fatigue syndrome"
Firslty many CFS/ME are TH2 dominant so the theory is inapplicable to many anyway.
You are right ,I may have separate depression - reactive or endogenous. (In fact most of my depression has been circumstantial and I do not respond well/normally to antidepressants).
It may to an extent, however, be a neuroimmune component of the ME/CFS as it might be in Lyme, B12 deficiency, B1 deficiency, toxoplasmosis etc . The clinical distinction has to be made because many CFS/ME do not have depression, as also many Lyme people do not have depression, but depression may be biologically entailed by Lyme in an individual and might also be biologically entailed in CFS/ME.
Further it depends what the theory is. If the theory is that "depression is universal in TH1 activated ME/CFS patients and is caused by serotonin depletion from diversion of tryptophan thru TH1 activation" then I agree. One non depressed patient confounds the theory.
It may nevertheless be the case in some sufferers.
the relationship may be complex. Time frames may play a role..E.g. TH1 produced excitotoxins sourced from tryptophan might actually deplete tryptophan but at the same time stimulate the brain to produce more serotonin from a depleted tryptophan reserve, which may make nutritional intake of trytophan or B3 important in symptom presentation.
lonfg term excitotoxicity might "fry" the brain causing depression AFTER the TH1 stimulation has gone.
My point is there is enough in immune disturbed states to theoretically create different physical and mental symptoms according to cause, genetics, circumstance, complications etc. This would not be controversial in a discussion of Lyme or B12 deficiency or toxoplasmosis or a host of other illnesses. It is controversial in our context because we fear psychologisation. But by refusing to discuss such matters we may be missing valid some insights - more valid for some , less for others.
You are right ,I may have separate depression - reactive or endogenous. (In fact most of my depression has been circumstantial and I do not respond well/normally to antidepressants).
It may to an extent, however, be a neuroimmune component of the ME/CFS as it might be in Lyme, B12 deficiency, B1 deficiency, toxoplasmosis etc . The clinical distinction has to be made because many CFS/ME do not have depression, as also many Lyme people do not have depression, but depression may be biologically entailed by Lyme in an individual and might also be biologically entailed in CFS/ME.
Further it depends what the theory is. If the theory is that "depression is universal in TH1 activated ME/CFS patients and is caused by serotonin depletion from diversion of tryptophan thru TH1 activation" then I agree. One non depressed patient confounds the theory.
It may nevertheless be the case in some sufferers.
the relationship may be complex. Time frames may play a role..E.g. TH1 produced excitotoxins sourced from tryptophan might actually deplete tryptophan but at the same time stimulate the brain to produce more serotonin from a depleted tryptophan reserve, which may make nutritional intake of trytophan or B3 important in symptom presentation.
lonfg term excitotoxicity might "fry" the brain causing depression AFTER the TH1 stimulation has gone.
My point is there is enough in immune disturbed states to theoretically create different physical and mental symptoms according to cause, genetics, circumstance, complications etc. This would not be controversial in a discussion of Lyme or B12 deficiency or toxoplasmosis or a host of other illnesses. It is controversial in our context because we fear psychologisation. But by refusing to discuss such matters we may be missing valid some insights - more valid for some , less for others.
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From my understanding is that pain and depression share the same neuro pathway? It would be interesting to know if people who also have FM are the ones experiencing depression? I've known 3 people personally with FM and all 3 suffer from depression as well.
High serotonergic CFS does not look unlike athletic overtraining, and alot of your abstracts are from the W school, Some might say that the cohorts may have included many burn out cases.
I have low serotonin (or have had). But I have also had had raised quinolinate, which might indicate brain inflammation, given the raised index of suspicion of brain inflammation in CFS/ME.. So am I poster boy for brain inflamed, excitotoxic real physical ME, on that basis or not ME/CFS on the basis of low serotonin.
These are the perils of purely symptomatic diagnosis.
Add tot hat that our biologies probably change over the years........
Here's some other views
http://www.ncbi.nlm.nih.gov/pubmed/15570154
http://chronicfatigue.about.com/b/2...-to-serotonin-in-chronic-fatigue-syndrome.htm
Are we one cohort?
I have low serotonin (or have had). But I have also had had raised quinolinate, which might indicate brain inflammation, given the raised index of suspicion of brain inflammation in CFS/ME.. So am I poster boy for brain inflamed, excitotoxic real physical ME, on that basis or not ME/CFS on the basis of low serotonin.
These are the perils of purely symptomatic diagnosis.
Add tot hat that our biologies probably change over the years........
Here's some other views
http://www.ncbi.nlm.nih.gov/pubmed/15570154
http://chronicfatigue.about.com/b/2...-to-serotonin-in-chronic-fatigue-syndrome.htm
Are we one cohort?
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Actually it's controversial because 1) the symptoms aren't at all similar, and 2) all biological research comparing CFS and depression has found them to be quite different, often diametrically opposite from each other.
Basically the entire theory has been more-or-less disproven, over several decades, yet a contingent still want to treat the depression theory as being very plausible, or even as a proven fact. Pointing that out is not a "fear of psychologization".
Basically the entire theory has been more-or-less disproven, over several decades, yet a contingent still want to treat the depression theory as being very plausible, or even as a proven fact. Pointing that out is not a "fear of psychologization".