amaru7
Senior Member
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@Valentijn before you jump into wrong conclusions, read first what the Wiki link states
Welcome to Phoenix Rising!
Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
To become a member, simply click the Register button at the top right.
I did read it. And I read the edit history. It has "Sciencewatcher's" grubby quack fingers all over it, just like the main CFS article.@Valentijn before you jump into wrong conclusions, read first what the Wiki link states
[...]evidence suggests that neurotransmitters excreted in the urine may have a place in clinical practice as a biomarker of nervous system function to effectively assess disturbances and monitor treatment efficacy.
There is a definite association between urinary and central neurotransmitter concentrations and many studies have examined that association through various neuro-endoimmune communication mechanisms.
Overall, urinary neurotransmitter analysis can be a useful tool in any clinical practice dealing with psychiatric disorders.
It is so not pointless.
A clinical situation
I have CFS for 30 years. No diagnosis for 13
I get tests ca 2000. TH1 activation clearly shows. Organic immune disturbance in fatigued patient (CFS/ME consistent over years)
Some reactive depression and natural anguish.
TH1 activity can deprive brain of tryptophan therefore causing endogenous depression, sleep probs etc. Armed with this knowledge of overlap I can request antidepressants (albeit in microdoses) without in any way conceding that I have depression rather than CFS/ME and allowing that the underlying cause of both may be the immune activation and/or autoimmune or infective processes underlying the immune activation, and NOT NECESSARILY STRESS RELATED..
Knowing the overlaps empowers us in the argument for physical causality and refutes who claim we are dualists , have no understanding of stress etc.
Could we please stop this once and for all?!
ME is not depression! Both are two complete distinct entities. The symptom patterns are remarkably different and quite easy to distinguish (except you like the Oxford criteria). Of course there is some overlap. Depressed patients can develop severe fatigue and sleep disruption. But this doesn't mean anything. MS patients can develop the same, but do we have therefore MS? No!! People with autoimmune hepatitis suffer from crushing fatigue. Do we have that, because of an overlap in one core symptom? No!! I could go on and on...
To make things even clearer:
Patients with depression have no PEM, no OI, no ataxia, no severe vertigo, no gastro paresis, no heat intolerance, no sore throat, no tender lymph nodes etc.
Also ME patients usually want to get back on their feet as fast as possible and want to study, work or meet friends etc. Most of us even know that activity will backfire with a crash (or better PEM), but do it anyways. Why? Because we have an intact will and still hope.
Severly depressed patients don't want to do much and cannot see any sense in their life. If you push them for any activity and especially sports it won't backfire at all. Usually it will improve the severe feelings of hopelessnes.
I don't stigmatize depression or any other mental disease. These patients have a horrible disease and deserve good care and treatment. The problem, the treatment, which helps depressed patients, doesn't work or is even harmful for us, like GET or CBT. It is like people don't treat depression with heavy immunosupressive drugs, because depression has some symptom overlap with MS. It's just nonsense.
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 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.
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. There are PWCFS with high serotonin. 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).
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.
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. There are PWCFS with high serotonin. 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).
That you had it does not mean others should have it too.
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.
I agree and the converse applies too.
I'd expect symptoms to show some similarities if the same pathways were involved.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.
My experience is that infection can knock out cortisol even in periods of garte biological stress. Isn't there much work on stages of adrenal failure, showing that eventually cortisol production can fail despite ongoing stress stimulation?
Didn't Louisa Scott fiind adreanl hypotrophy in her patients at Kings (albeit under Wessely. I think)? Dr Wrightt showed me her paper and he was no frioend of the psychologisers.
Studies suggest that adrenal atrophy due to hypothalamic-pituitary disease or corticosteroid therapy is associated with greater impairment of DHEA and DHEA-S than the secretion of cortisol, and that the capacity to secrete cortisol recovers more rapidly than the capacity to secrete the DHEAS when corticosteroid therapy is withdrawn (Cutler et al., 1979). The clinical implication of this in CFS is that the administration of hydrocortisone as a therapeutic measure in CFS (Doepal, 1996 and Cleare et al., 1998) may be further lowering the levels of DHEA and DHEA-S. The present study would suggest that a trial of DHEA in the treatment of CFS is warranted.
I have had reactive deprsssion and possiblly endogenous depression, the latter due to immune mediated serotonin deficiency, possibly due to a brain blown for years out on TNF alpha and other physiologial factors and my problem has been fatigue/fatigability always. depression sometimes.
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.
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"
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.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.
My aunt and neighbor both have FM. Neither seem depressed - both stay busy with work/volunteering, family, pets, etc, and are typically upbeat when I talk to them.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.