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Chronic Fatigue - Prozac

144 posts in this topic

http://www.bollyn.com/how-do-ssri-antidepressants-work

 

 Drastic rise in blood pressure and cholesterol levels, severe loss of memory, hair loss, sleep disorders, headaches, joint pain, muscle contractions, sweating, nausea, severe abdominal pain (often a burning pain), kidney pain and kidney failure, burning urination, hypoglycemia, diabetes, abnormal liver function, development of various allergies, rashes, development of Chronic Fatigue Syndrome symptoms, chronic digestive problems including poor metabolism, indigestion, gas and diarrhea, ulcers, blurred vision, electric surges shooting throughout the head and body (similar to what is known as "post drug syndrome"), slurred speech, adrenalin rushes at the slightest provocation, seizures, sexual dysfunction, bloating and weight gain, endless ringing in the ears, burning or tingling in feet or legs, swelling in joints, heart flutter, and heart attacks.

 

After taking Prozac  less than a month... I developed Chronic Fatigue.  I have been trying to make connection to this for 30 years.. 

as in mitochondria damage is part of chronic fatigue and prozac causes mitochondrial damage.  I know I did not have it before prozac 

and that I had it after prozac.  

 

I had one lady on PP talk with me about this once I really don't hear much about it at most site so was very interested in this site. 

There are a few other things that I have suspected or heard of rarely on other sites.  I will be watching this one.  As I think they are on

the right track ahead of the rest. 

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It only took a month for you to get CF from Prozac?

 

Why are these drugs still around?

 

Ugh. 

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Chronic fatigue is an issue for me as well, though I have not as of yet had it diagnosed. I also was not fatigued before I restarted Celexa.

 

My thoughts on what happened is that my nervous system was so revved up in such a severe way for so long that eventually it crashed, leading to fatigue. 

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I got chronic fatigue from prozac. as I go lower on dose it is getting better though, slowly. your's didn't improve after removing prozac?

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It only took a month for you to get CF from Prozac?

 

Why are these drugs still around?

 

Ugh. 

I just learned today I was on 3x the recommended starting dose... learned it here

http://www.bollyn.com/school-shootings/

no wonder I had such a bad reaction. 

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The horror of taking the drug... changed who I am.  The fallout was a year later I was sill messed up could not sleep could not get up... doing the bare minimum for survival and still in pain. 

I eventually went to a pain clinic where they put me on a tricyclic  antididepressant called amitriptyline ... I started the drug before I went into the pain clinic about a wk before but it was ordered by the pain specialist at the clinic when I was there to be assessed. I slept around the clock... I took it for a few years at a very low dose... was on the lowest dose possible and still I had to take it after dinner in order to be awake the next day... after dinner I could not see to watch tv...or read my eyes were so blurry.  

I was mostly a sleeping zombie not really living... when my mother got cancer and came to live with me for treatment I could not keep up zoloft was added( for me zoloft was energizing and brought impulsive thoughts of crashing the car)... after she died I tried to get off them both ... too fast taper according to the doctors schedule ... enter paxil... which I reacted badly too... if hiding in the closet and extereme fear is not a favourable response...ack hated paxil and prozac...immediately... 

and on I went.. more and more.. till 18 years of my life were eaten up... 

 

I don't know if chronic fatigue is playing a part all these years who can tell with all the crap I have been thru... who knows if they were right in the dx... I know that is what I was told.  

 

To me at this point in my life whatever a doctor says is suspect... sorry if that does not sit well with others is is what I have deemed part of my survival plan.  Some of what they say may be corrected based on symptoms ...until they take into account the affects of the drugs...ALL of the affects they could not possibly have a correct dx... and they don't know... so how is it possible it isn't is my determination.  They can see the symptoms and the signs left behind to a certain extent but they can't say how they got there... and without knowing the cause how good will their treatment be.  

 

So I fly by the seat of my pants... weigh things out for myself and wait... I do a lot of waiting as time is an amazing qualifier... and our bodies are trying to heal all the time.  We need to attend to the needs of our bodies whatever they are at any given time and during this process the needs change.  

 

It is a day by day thing... we are changing as I speak. 

peace all.

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btdt, did they test you for sleep problems at a sleep clinic before getting the diagnosis?

 

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They did a sleep deprived EEG that came out wonky they said I was alseep when I was not asleep...my brain was asleep but I was awake.  I have had sleep tests just now the order they were done is a bit clouded in my mind.  I will let it sit and it will come to me as the day goes on. 

 

For the test I recall I had to stay awake all night.  I went to the hosp they did the test.  After the test the lady came in and asked me if I had a nice nap... I said "I did not sleep at all why are you saying that"  She said you brain was asleep.  This was long time after prozac before the pain clinic and before I was given any other drugs... I was still suffering from the severe adverse reaction from 2 wks of 60mg of prozac...call it severe adverse reaction or withdrawal .. it was bad. 

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I have talked about this result with a person called iwowi at the other site she had the same test I think... and had a name for it ...

I think there may still be a thread at the other site under that name tho all my input will be deleted... 

She was given this name

Sleep state misperception ... close as I can recall... I could be wrong.

not sure if Alto allows this but here is the link... guess it is one way of finding out.... sorry Alto if I am on the list

http://www.paxilprogress.org/forums/showthread.php?t=39369

 

more too

https://www.google.ca/search?q=paxilprogress.org+-+%22sleep+state%22&oq=paxilprogress.org+-+%22sleep+state%22&aqs=chrome..69i57.12594j0j1&sourceid=chrome&ie=UTF-8

 

you can always search the site  yourself... 

I feel I just did something wrong but really who's work it is it is ours...

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Sleep state misperception, I am familiar with that.

 

I may have had that to some degree in a sleep test I had as well.  Wonder what can be done about it.

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There is apparently a stage of sleep that chronic fatigue folks don't get.. I do not know that this is true but it is in my head... 

found this bit

Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a chronic, disabling illness that affects approximately 0.2% of the population. Non-restorative sleep despite sufficient or extended total sleep time is one of the major clinical diagnostic criteria; however, the underlying cause of this symptom is unknown. This review aims to provide a comprehensive overview of the literature examining sleep in CFS/ME and the issues surrounding the current research findings. Polysomnographic and other objective measures of sleep have observed few differences in sleep parameters between CFS/ME patients and healthy controls, although some discrepancies do exist. This lack of significant objective differences contrasts with the common subjective complaints of disturbed and unrefreshed sleep by CFS/ME patients. The emergence of new, more sensitive techniques that examine the microstructure of sleep are showing promise for detecting differences in sleep between patients and healthy individuals. There is preliminary evidence that alterations in sleep stage transitions and sleep instability, and other physiological mechanisms, such as heart rate variability and altered cortisol profiles, may be evident.

Future research investigating the etiology of non-restorative sleep in CFS/ME may also help us to undercover the causes of non-restorative sleep and fatigue in other medical conditions.

 

I would not be too surprised to see this change ... not sure about anything where this dx is concerned... actually it could be many things... science will catch up one day and we will find out.

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I think there must be different causes. Trouble with us is if the drugs are to blame (and in my case at least I feel they are) then how likely is it they will try to unravel what they do?

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btdt, I was reading about a possible herbal remedy for standard CF which I may try.  I am going to sit with this idea for a bit and see if I can't intuit if it would be a good idea or not.  What I have read about it is it tends to cause a healing crisis at the outset of treatment so that is my big concern, but if I try it I will use a teeny fraction of the dose and see what it does. 

 

I'll report back with my results if it's a go.

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I think there are different causes too maybe with an underlying similar issue or maybe these are two different things that present the same.  I have read a lot about adrenal fatigue too... however I was not the one that did the research and found chronic fatigue is associated with mitochondria disorders or that prozac among other drugs can cause mitochondria disorder... I just happened to notice it. 

I don't know about creating a healing crisis that does not sound conducive to healing withdrawal it sounds like setting your body back.  I just don't know.  I read one time that antidepressants help people by causing injury and that the bodies healing of the drug induced injury is what was giving study results that they are good for the brain... 

Way to complex for my brain. 

My gut on the other hand says Its not nice to fool with mother nature... but I could be dead wrong.  

Is there any understanding of how it works or just a lot of reports that it does work.  

Even while I say this I did tinker with this and that and try to get my system to come back online when I was suffering severe fatigue. I tried various vitamins and the only supplement I will take now has an odd story.  I was trying taurine to treat mirgraine and found it worked for the physical type of anxiety... edginess. I get from too much coffee or coffee on a day when I should have had no coffee. 

Follow you own gut and do take a very small amount ... one of the best things I have learned on the computer small doses... that has save me plenty I suspect. 

peace.. U

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So far what I have read about the herb are reports and a little about what it was historically used to treat.

 

I don't know if there is info on how it works at this time.  Often with herbs the historical info is much more detailed than the scientific.  Although there are studies for some--but they can be full of problems like drug studies often are.

 

That is partly why I am trying to do this intuitively.  At present moment I have no sense one way or another whether I should take it or not.  But it would be a miracle if they had even one study about how it affects people like us.

 

Also I forgot to mention thanks to cog fog that part of my fatigue was caused by a mild iron deficiency.  I have treated it though and last time I was tested my levels were supposedly okay.  So that can't account for the ongoing fatigue.

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Yes I was told if anything my iron was high. 

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So it looks like for both of us something else is going on.

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If you mean something other than iron yes 

Do these drugs cause chronic fatigue I think it should be raised as a question as to what the fallout is of the drugs that do damage mitochondria...I know prozac does and there are a few other ssris on the list and more each time I check the list....  it maybe damaged mitochondria respond differently depending on what caused the damage and damage is a very broad term... is the damage the same?  

To date as far as I know these questions have never been addressed.

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here is a bit of a story a comment on a this post here

 

 

"I am on my eleventh year with a serious metabolic disturbance from making the mistake of taking 1/2 to 1 mg daily dosage of risperdal back in 2001. The misinformation concerning these drugs has created something of a crackhouse environment way of conducting psychiatry today. In anycase the following quote comes from an article "Depression: a metabolic perspective" Richard Fiddian Green 27 October 2012, BMJ. Its interesting that a simple accurate factual voice (R.F. Green's voice that is) on what anti depressants and antipsychotics really do in the real world shows up in the British Medical Journal. Why such common sense approaches does not show up with the APA is bewildering? In anycase here is the quote:

"Conventional drug therapy leaves much to be desired from the metabolic perspective and needs to be re-evaluated with some urgency. If administered to persons whose capacity fro replenishing intraglial glycogen and intraglial and intraneuronal ATP stores is impaired mood elevators that act by enhancing neurotransmitter release and increasing the slope of neuron action potentials may compound the severity of the energy deficit present by increasing the demand for ATP hydrolysis beyond the capacity to replenish ATP stores. Any severity of any energy deficit present is likely to be compounded by those antidepressants that impair mitochondrial oxidative phosphorylation. It might also be compounded by drugs used to treat co-existing cardiovascular disorders, notably beta blockers and statins. Of great concern is that any medication or mixing of medications that either induces or compounds the severity of an intracerebral energy deficit might increase the likelihood of developing neurodegenerative disorders in later years especially if the medications are administered for extended periods." end quote.

The above from 2003 is a simple factual illustration of the cause and effects of anti depressants and antipsychotics on a patient's metabolic profile. Yet it seems the APA has trouble addressing these facets of the medications while all the other scientific and medical journals and research studies thankfully honestly relate the implications and nature of what the neuroleptics do. Kafka's cockroach may be running the APA these days, who knows."

 

about spells it out but does not say how to fix it since he has had it 11 years guess he has not found a cure either... 

http://thelastpsychiatrist.com/2012/10/if_psychiatry_is_committing_su.html 

posted by Harry Horton if you want to find the exact post

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Glutamate – One More Piece in the Chronic Fatigue Syndrome (ME/CFS) Puzzle?

 

(In a second of four-part series of papers elucidating a neuro-inflammatory model of chronic fatigue syndrome, Marco examines a possibility that could explain many symptoms and issue not just in ME/CFS but in other neurological disorders. Learn more about Marco here - Cort).  Pt 1 of the Neuroinflammatory Series: Not Fatigue After All: New Model Suggests Other Symptoms Better Explain Chronic Fatigue Syndrome (ME/CFS)  Glutamate Could glutamate excitotoxicity be a key player in chronic fatigue syndrome? Glutamate plays a beneficial and indeed crucial role as the  primary excitatory neurotransmitter powering the transmission of messages between neurons. Without glutamate we’d be unable to respond quickly to events but too much glutamate can lead to a condition called excitotoxicity which can damage or destroy neurons. “Excitotoxicity is the pathological process by which nerve cells  are damaged and killed by excessive stimulation by neurotransmitters such as glutamate…. This occurs when receptors receptors for the excitatory neurotransmitter such as the NMDA and AMPA receptors  are overactivated.” Wikipedia Interestingly, given the low blood flow problems in chronic fatigue syndrome, central nervous system ischemia (low blood flows) increases glutamate levels and contributes to cellular death. High glutamate levels shift the central nervous system towards seizure, and indeed, researchers have known for over 50 years that directly applying  glutamate to the central nervous system causes seizures.  Dr. Paul Cheney has long proposed that a shift towards seizure brought on by overstimulated, overly sensitive  neurons  explains the ‘wired but tired’ symptoms and sensory overload often  experienced in ME/CFS. “Our neurons (nerve cells) are sensing stimuli and firing when they should not. This causes amplification of sensory input. Light, noise, motion and pain are all magnified. At the beginning of their illness, many patients report feeling exhausted, yet also strangely “wired.” The “wired” feeling is the slight shift towards seizure that occurs as a result of the excitatory neurotoxicity.” From Carol Sieverlings reports Cheney proposed that overly activated NMDA (glutamate) receptors cause neurons to fire at the slightest stimulation.  He suggested people with ME/CFS use Klonopin,  Doxepin elixir and magnesium to reduce receptor activation and indeed Klonopin is widely used in ME/CFS. Normally glutamate is balanced by the inhibitory neurotransmitter GABA.  It is likely that the balance between glutamate and GABA may determine the excitatory/inhibitory balance in the central nervous system and hence the ratio of ‘signal’ to ‘noise’.  It seems logical that an excess of glutamate might result in increased noise and a deficit in signal gating leading to various ‘overload phenomena’. Evidence For Excessive  Glutamate in Chronic Fatigue Syndrome Links with Other Disorders In addition to an inflammatory milieu, oxidative stress and mitochondrial dysfunction (all of which interact),  diabetes is a final condition not discussed as yet (and for which no research has been conducted on sensory gating) but which may hold a clue to glutamate as a key driver involved in ME/CFS and other neuroinflammatory conditions. You may recall that the CDC (Maloney et al, 2010) suggested an association between metabolic syndrome (a precursor to type II diabetes) and ME/CFS, albeit in a study using the empirical criteria.  Recent research has identified excess glutamate as a potential mechanism leading to the onset of type II diabetes via the destruction of pancreatic cells by glutamate (Eliana et al, 2011). Kogelnik, in an interview coming up,  has reported increased levels of diabetes in his chronic fatigue syndrome patients. This suggests excess glutamate could be triggering sensory gating problems, diabetes and mood disorders in some patients.  Type II diabetes rates are three times higher in patients with bipolar disorder compared to the general population(Calkin et al 2012).  In the same vein it’s intriguing that diabetic mothers have a higher risk of having children on the autism spectrum (Krakowiak et al, 2012). . Notably excess glutamate has also been implicated in most if not all of the conditions discussed here including ME/CFS - indirectly via allostatic load (Goertzel et al, 2006) and the concept of the ‘selfish brain’ (Peters et al, 2004). Glutamate’s key role in neuronal plasticity suggests it could help remodel the nervous systems in people with ME/CFS. Murrough (2010) did not find altered levels of glutamate or GABA in an ‘exploratory’ analysis of ME/CFS patients.  However increased central nervous system glutamate levels have been well-documented in fibromyalgia patients and a study analysing the effects of a glutamate blocker called memantine on pain and glutamate levels is underway.  Australian researchers propose that inactivation of  glutamate limiting  enzyme called GAD plays a key role in FM, and note that being female, poor sleep, sedentariness, anxiety and depression can all depress GAD functioning. Interestingly, given the alcohol intolerance in ME/CFS, alcohol depresses GAD functioning as well.

 

Read more: Glutamate – One More Piece in the Chronic Fatigue Syndrome (ME/CFS) Puzzle? The Neuroinflammatory Series Pt. II http://www.cortjohnson.org/blog/2013/02/15/glutamate-one-more-piece-in-the-chronic-fatigue-syndrome-mecfs-puzzle-the-neuroinflammatory-series-pt-ii/

 

 

Evidence For Excessive  Glutamate in Chronic Fatigue Syndrome Links with Other Disorders In addition to an inflammatory milieu, oxidative stress and mitochondrial dysfunction (all of which interact),  diabetes is a final condition not discussed as yet (and for which no research has been conducted on sensory gating) but which may hold a clue to glutamate as a key driver involved in ME/CFS and other neuroinflammatory conditions. You may recall that the CDC (Maloney et al, 2010) suggested an association between metabolic syndrome (a precursor to type II diabetes) and ME/CFS, albeit in a study using the empirical criteria.  Recent research has identified excess glutamate as a potential mechanism leading to the onset of type II diabetes via the destruction of pancreatic cells by glutamate (Eliana et al, 2011). Kogelnik, in an interview coming up,  has reported increased levels of diabetes in his chronic fatigue syndrome patients. This suggests excess glutamate could be triggering sensory gating problems, diabetes and mood disorders in some patients.  Type II diabetes rates are three times higher in patients with bipolar disorder compared to the general population(Calkin et al 2012).  In the same vein it’s intriguing that diabetic mothers have a higher risk of having children on the autism spectrum (Krakowiak et al, 2012). . Notably excess glutamate has also been implicated in most if not all of the conditions discussed here including ME/CFS - indirectly via allostatic load (Goertzel et al, 2006) and the concept of the ‘selfish brain’ (Peters et al, 2004). Glutamate’s key role in neuronal plasticity suggests it could help remodel the nervous systems in people with ME/CFS. Murrough (2010) did not find altered levels of glutamate or GABA in an ‘exploratory’ analysis of ME/CFS patients.  However increased central nervous system glutamate levels have been well-documented in fibromyalgia patients and a study analysing the effects of a glutamate blocker called memantine on pain and glutamate levels is underway.  Australian researchers propose that inactivation of  glutamate limiting  enzyme called GAD plays a key role in FM, and note that being female, poor sleep, sedentariness, anxiety and depression can all depress GAD functioning. Interestingly, given the alcohol intolerance in ME/CFS, alcohol depresses GAD functioning as well. Glutamate antagonists N-acetylcsysteine (NAC) is usually thought of as an antioxidant but it also  acts as a glutamate antagonist through facilitating the production of GABA.  A number of small clinical trials have shown promising results for NAC administration in another disorder with sensory gating issues,  Autism Spectrum Disorder (ASD) (Hardan et al, 2012).  NAC is also fairly well established in the treatment of trichotillomania  (compulsive hair pulling – a form of obsessive compulsive disorder (OCD). NAC’s effectiveness  in ameliorating a sensory gating deficit may therefore lie in its role as a glutamate antagonist instead of (or indeed as well as) its antioxidant properties and role as a glutathione precursor. Oral GABA supplementation has also been shown to have potential to prevent metabolic syndrome and type II diabetes in a mouse model (Tian et al, 2011).  Even more promising, neuronal damage caused by glutamate in ASD may be reversible by attenuating the over proliferation of glutamate receptors in the brain (Baudouin et al, 2012). Another glutamate inhibitor, low dose naltrexone (LDN) has shown some efficacy with pain and mood in fibromyalgia. Dig Deeper: For more on low dose naltrexone, fibromyalgia and chronic fatigue syndrome  Glutamate and ‘Neuroinflammation’ In fact, research is increasingly suggesting that oxidative stress, mitochondrial dysfunction and glutamate excitotoxicity are intrinsically linked in a range of neuroinflammatory conditions (Coyle and  Puttfarcken, 1993) presenting as various symptom complexes “Thus, two broad mechanisms–oxidative stress and excessive activation of glutamate receptors–are converging and represent sequential as well as interacting processes that provide a final common pathway for cell vulnerability in the brain. The broad distribution in brain of the processes regulating oxidative stress and mediating glutamatergic neurotransmission may explain the wide range of disorders in which both have been implicated. Yet differential expression of components of the processes in particular neuronal systems may account for selective neurodegeneration in certain disorders.” In short, the same pathological process can result in a different constellation of symptoms and therefore result in a range of eventual diagnoses. Oxidative stress, mitochondrial dysfunction and glutamate excitotoxicity may also interact as a ‘feed-forward’ vicious cycle (Nguyen et al, 2011) : “Our results conclusively demonstrate that not only glutamate excitotoxicity and/or oxidative stress alters mitochondrial fission/fusion, but that an imbalance in mitochondrial fission/fusion in turn leads to NMDA receptor upregulation and oxidative stress. Therefore, we propose a new vicious cycle involved in neurodegeneration that includes glutamate excitotoxicity, oxidative stress, and mitochondrial dynamics.” Stablon (tianeptine) is an atypical antidepressant that has demonstrated remarkable clinical effectiveness in major depressive disorder that is often resistant to treatment with traditional SSRI’s.  The interesting fact about tianeptine is that its efficacy does not conform to the monoamine hypothesis of depression as tianeptine may actually lower serotonin levels.  An investigation into the neurobiological properties of tianeptine (McEwen et al, 2010) concludes : “Converging lines of evidences demonstrate actions of tianeptine on the glutamatergic system, and therefore offer new insights into how tianeptine may be useful in the treatment of depressive disorders.” Intriguingly the antidepressant and anxiolytic effects (plus protection against cognitive defects) appear to be due to its ability to protect the brain (particularly in the amygdala and hippocampus) against stress induced glutamate excitotoxicity : “A modification of glutamatergic mechanisms by tianeptine may therefore be implicated in its ability to oppose the negative influence of chronic stress upon hippocampal neurogenesis, cell proliferation, and dendritic remodeling, processes profoundly disrupted in depressive states” Dig Deeper: More on Tianeptine (Stablon) and chronic fatigue syndrome (ME/CFS) Similarly ketamine has a rapid and sustained antidepressant effect through modulation of glutamate neurotransmission as does the novel compound GLYX-13 which has the same beneficial effects without inducing dissociative symptoms usually associated with schizophrenia (Burgdorf et al, 2012) Dig Deeper: More on Ketamine, Fibromyalgia and pain reduction Mental Fatigue Wrapped up within the vague notion of ‘fatigue’ in ME/CFS is the rather more specific description contained in the Canadian Consensus Criteria of a “Low threshold of physical and mental fatigability (lack of stamina)”.  Mental fatigue is a common symptom following brain trauma and encephalitis and is associated with a number of neuroinflammatory and neurodegenerative disorders and can also result from sleep deprivation.  Ongoing research at the University of Gothenburg, Sweden has implicated glutamate dysregulation in mental fatigue (Rönnbäck,  Hansson, 2004) which they define as  : “a decreased ability to intake and process information over time. Mental exhaustion becomes pronounced when cognitive tasks have to be performed for longer time periods with no breaks (cognitive loading).” and : “In addition to the fatigue itself, the patient with mental fatigue often suffers from loudness and light sensitivity, irritability, affect lability, stress intolerance, and headaches” The researchers’ University of Gothenburg home page also describes over-exertion leading to a state of mental “deadlock” : “Intense mental activity with high glutamate signalling can lead to astrocytes swelling, especially if their glutamate uptake capacity is impaired. This state, which is locked, may resemble the feeling of cramp in a muscle and the signalling takes a long time to be restored. This may explain the total exhaustion experienced by a person suffering from mental fatigue, when being too active and doing too many things.” Rönnbäck and Hansson propose an inflammatory state where the efficient transmission of information via glutamate is disrupted with a decrease in the ability to discriminate signal from noise; in effect, the sensory filter ‘disintegrates’ : Cytokines associated with chronic fatigue syndrome could help produce the sensory overload and fatigue in the disorder “Based on this literature and observations from our own laboratory and others on the role of astroglial cells in the fine-tuning of glutamate neurotransmission we present the hypothesis that the proinflammatory cytokines tumor necrosis factor-α, IL-1β and IL-6 could be involved in the pathophysiology of mental fatigue through their ability to attenuate the astroglial clearance of extracellular glutamate, their disintegration of the blood brain barrier, and effects on astroglial metabolism and metabolic supply for the neurons, thereby attenuating glutamate transmission.” TNF-a and IL-6 have, in separate studies, both been identified as potentially key immune factors in ME/CFS The authors go on to note that, in some cases, mental fatigue persists long after the identified neural trauma has been resolved (perhaps due to a genetic predisposition or due to dendritic remodelling) and emphasise the importance of early treatment to prevent the problem becoming chronic : “Providing information about mental fatigue, its cause and the prognosis, is of utmost importance for breaking the vicious circle, which comes with the risk for secondary anxiety and depression. Furthermore, it is important for the patient to imagine and learn how much sensory stimulation they can tolerate prior to feeling too exhausted. Due to recent results on changes in cell signaling and neuronal plasticity, it may be important to identify the symptoms and treat them as early as possible to avoid formation of new and functionally disturbing neuronal circuits due to overstimulation of neuronal-glial units.

 

Read more: Glutamate – One More Piece in the Chronic Fatigue Syndrome (ME/CFS) Puzzle? The Neuroinflammatory Series Pt. II http://www.cortjohnson.org/blog/2013/02/15/glutamate-one-more-piece-in-the-chronic-fatigue-syndrome-mecfs-puzzle-the-neuroinflammatory-series-pt-ii/

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posted too much I think there is so much more and none of it will go into my head... some other day I will get it

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http://www.rlcure.com/glutamate2.html

Lowering glutamate naturally ...not food which I was hoping for but shows some food restrictions and talks of taurine which I do use on occasion.  The other interesting bit was on inflammation. 

 

"

Be careful when you read studies. You never know what the author's motive may be or who may be backing the study. Dr Amy Yasko does not recommend l-glutamine because it can turn into glutamate, especially if the GAD gene or enzyme is affected in any way. 

And certainly be aware of any dietary influences, especially MSG (it goes without saying). Peas, mushrooms and Parmesan cheese are also on the high glutamate avoid list. "

 

"

After taking everything I've learned into consideration, my recommendation is to take neither the supplement GABA or L-Glutamine. 

Because of the inflammation in your body, their behavior in the delicate Glutamate-glutamine cycle is unpredictable. My suggestion is to take L-Theanine or Taurine and to also consider some of the other natural GABA boosters you'll read about below."

 

I personally will stick with taurine as I already know I do well with it.  

 

"Calcium is another factor in the glutamate GABA story. If glutamate is like a gun, then calcium is the bullet. Glutamate creates the scenario for excitotoxicity to happen, but the agent that actually destroys the nerve cell is the influx of calcium. The combination of excessive glutamate from any source and too much calcium is major. "

 

" using zinc to limit glutamate damage"

 

I may try the zinc... maybe

you can read more of this here if you have interest.

http://www.rlcure.com/glutamate2.html
 

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Too early to gauge if this is successful or just a coincidence, but, I may have stumbled on something that helps drug-induced fatigue.

 

Yesterday I had a very inflammed gum.  I have jaw issues and can't often open my jaw very wide so going to a dentist could be problematic.  So I looked up what else I could do to get rid of it and found oil pulling.  I tried it with coconut oil.

 

I had forgotten that I had bought some as I read it helps hypothyroidism and for a while I wondered if maybe that was the cause of my fatigue.  At the time I didn't want to go to the doctor for obvious reasons, but later did get it tested and apparently I don't have it (whether the tests were thorough enough though I don't know.) 

 

Anyway, last night I used the oil and then rinsed with salt and my gum is now almost back to normal.  But an interesting thing happened, I also woke up with way more energy than I normally have and didn't oversleep.  Some of it was a bit of that edgy drug-induced restlessness, so it wasn't all great, but it wasn't severe and has abated.  Still feel far more energetic than normal.

 

The only things I have changed recently is last night I went for a decent walk, and I did the oil pulling.  Normally if I go out for a walk it might help with sleep but I will be so exhausted the next day that it makes me want to never do it again.  So it seems possible the oil pulling may be responsible since it's likely I ingested tiny amounts of coconut oil while doing it.

 

I haven't read the studies mentioned online about its use for chronic fatigue, though I am pretty sure there is something to its use for hypothyroidism (though I don't think using it alone is a total solution.)

 

One caveat though, if it is helpful for hypothyroidism then it won't be good for people who are hyperthyroid or who have conditions where they can go hyperthyroid.  Nor would it likely be a good thing to take if you currently have akathisia or severe restlessness/anxiety.  And as with all things in withdrawal, less is more; I took only a fraction of a teaspoon.

 

I'll keep it up and see if benefits continue. 

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btdt, I was reading about a possible herbal remedy for standard CF which I may try.  I am going to sit with this idea for a bit and see if I can't intuit if it would be a good idea or not.  What I have read about it is it tends to cause a healing crisis at the outset of treatment so that is my big concern, but if I try it I will use a teeny fraction of the dose and see what it does. 

 

I'll report back with my results if it's a go.

 

Well, I'm back to say, way after the fact, that I finally tried it.

 

So far it has gone okay.

 

Took a bit yesterday and not too long after felt I could concentrate better, also seemed to have more energy, but not in a revved up sort of way.

 

Now I took a larger amount today and again feel better.

 

I was having a problem which someone else mentioned where it seemed my unconscious was "too loud", like it was too much at the forefront of my mind.  Now it's receded.  I haven't the faintest idea how it did that but it has.

 

Also, and this was unexpected, it seems to be helping my mood, which was okay prior to drugs (long story, I had some situational problems going on then but wasn't always down, I disagree with the diagnosis of "depression" I got) but now has been badly damaged by the drugs.  I am not sure why, but it seems to have made me feel better in that department.

 

And, yesterday I was starting to get back some memories I had not thought of in years, just vague ones, but still stuff that is more positive that I hadn't thought of in a long, long time.  My brain tends now to get lodged on one subject and won't move, often it's negative though not always now that I am partly recovered...But yesterday it seemed more fluid.

 

So so far so good, will update...but it does seem to work for fatigue.

 

Big caveat of course is I am not sure how it would affect others; I found it took years for me to be able to tolerate herbs again and still I have to be cautious.  But a few i can take regularly and they don't bother me.

 

Oh and it seems to be helping IBS too, which is one of the things it's supposed to help...So so far I am impressed, feeling better than I have in a long while.

 

Hopefully this isn't going to turn on me in a few days though.  Will update one way or another. 

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Glad it is helping you :) good news.

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Thanks btdt, hopefully it continues to work.

 

And hope you are doing better too. :)

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Thanks UFS I think I need a vacation :) after I get better and off the steroids.  

I bet a lot of us on here could use a vacation. 

I had thought of banning myself from here till I am done the steroids trying to not say the wrong thing as I am on the bitchy side...so if I seem short that would be it that is why I hate them i so react to all drugs... it sucks I am guarded...but this too will pass I am getting better again.  

thank you for asking 

peace

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Hey no problem.  I am sorry the steroids are giving you a runaround.  Yeah no doubt we all could use a vacation...I could do without the cabin fever winter brings. 

 

Praying for your speedy recovery,

 

US

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Thank you seems I have had the flu twice this month if i am to believe clinic doctors sometimes i think they will say any old thing to get people out the door faster as the clinics are so backed up. 

I am going to start using less maybe even quit taking them tomorrow and hope for the best.  fingers crossed. 

peace

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Hope your "flu" cleared up btdt, need to come check out your thread. :)

 

So, my update about the herb--it seems to help with some stuff but it may be that it only minimally helps with fatigue.

 

Go figure.

 

Strangely, it has really, really helped with cognitive issues.  I am still not a hundred percent but after taking it there is a sharp and noticeable difference.  I decided to lay off it for a few days and then try it again just to see what would happen...Took it today and oh my gosh the difference it makes.  You can actually feel the fog start to lift.

 

Now, WHY it's doing that I have no idea.  It is said to help strengthen the immune system so maybe that has something to do with it.

 

It's also listed as an anti-inflammatory.  I know there's some newer argument about "depression" being due to inflammation, haven't looked into that at all as i know some of what is labeled as "depression" is from other stuff, so don't believe in one big theory to account for all of it.

 

And I didn't have "depression" going into this either, long story (though that was officially why I was put on ADs.)

 

Does anyone know of any credible info that suggests withdrawal particularly or adverse drug reactions cause some sort of inflammation?
 

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Hope your "flu" cleared up btdt, need to come check out your thread. :)

 

So, my update about the herb--it seems to help with some stuff but it may be that it only minimally helps with fatigue.

 

Go figure.

 

Strangely, it has really, really helped with cognitive issues.  I am still not a hundred percent but after taking it there is a sharp and noticeable difference.  I decided to lay off it for a few days and then try it again just to see what would happen...Took it today and oh my gosh the difference it makes.  You can actually feel the fog start to lift.

 

Now, WHY it's doing that I have no idea.  It is said to help strengthen the immune system so maybe that has something to do with it.

 

It's also listed as an anti-inflammatory.  I know there's some newer argument about "depression" being due to inflammation, haven't looked into that at all as i know some of what is labeled as "depression" is from other stuff, so don't believe in one big theory to account for all of it.

 

And I didn't have "depression" going into this either, long story (though that was officially why I was put on ADs.)

 

Does anyone know of any credible info that suggests withdrawal particularly or adverse drug reactions cause some sort of inflammation?

 

Yes there is something that goes up when we are on these drugs that goes down when we are off... whatever it is that goes up... has an anti inflammatory affect. 

I can't think of what it is but I will look. 

I can't find it.. not yet I saved it on another site which is now gone... I am still looking tho. 

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A comparative examination of the anti-inflammatory effects of SSRI and SNRI antidepressants on LPS stimulated microglia.

. Accordingly, the current study evaluated the ability of five different SSRIs (fluoxetine, sertraline, paroxetine, fluvoxamine and citalopram) and one SNRI (venlafaxine) to suppress microglial responses to an inflammatory stimulus. Specifically, we examined their ability to alter tumour necrosis factor-α (TNF-α) and nitric oxide (NO) production after 4 and 24 h stimulation with lipopolysaccharide. Our results indicated that the SSRIs potently inhibited microglial TNF-α and NO production. We then investigated whether these effects might involve either β-adrenoceptor or cAMP signalling. Using the protein kinase A inhibitor Rp-CAMPs, we found evidence to suggest that cAMP signalling is involved in regulating the anti-inflammatory response. These findings suggest that antidepressants may owe at least some of their therapeutic effectiveness to their anti-inflammatory properties.

 

here is the link I don't think I can post the whole thing as I get trouble for that..

 

http://www.ncbi.nlm.nih.gov/pubmed/22251606

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From there here are some other ideas.

 

SSRIs) paroxetine and sertraline significantly inhibited the generation of NO and tumor necrosis factor (TNF)-α from interferon (IFN)-γ-activated 6-3 microglia. We further investigated the intracellular signaling mechanism underlying NO and TNF-α release from IFN-γ-activated 6-3 microglia. Our results suggest that paroxetine and sertraline may inhibit microglial activation through inhibition of IFN-γ-induced elevation of intracellular Ca2+. Our results suggest that the inhibitory effect of paroxetine and sertraline on microglial activation may not be a prerequisite for antidepressant function, but an additional beneficial effect.

http://www.sciencedirect.com/science/article/pii/S0278584610002769

and

http://f1000.com/prime/716598067

and

file:///C:/Users/sandy/Downloads/TYNAN%202012.pdf

 

This from a website looking to help

http://forums.phoenixrising.me/index.php?threads/chronic-microglial-activation-in-me-cfs-and-its-possible-treatment-using-microglial-inhibitors.34164/

 

I can't say I get it cause i don't I can look stuff up just now but nothing is getting into my head much today.  I am sorry to leave you on your own as there was a time I would be gobbling this up.  Sorry hope it makes some sense to you. 

peace

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If you look at all this with a brain that works at a lower percentage than normal... imply implications from other things one has learned by living a life and take into account the symptoms lived with personally ... it would point to these drugs being the cause of auto immune disorders.  At least I think it could as I am describing myself and found myself looking at this one ...if it involved the gut and lungs I would say this is what I have today... based on my history and currant life. 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2500254/

Now since we are always warned or were at pp not to let the health anxiety get the better of us and beware of googlitis as a further complication of wd... it is hard to say which it is today. 

Either while I wish to be in top form and seek answers I know my brain is not functioning well enough to actually do it and the affect it has on how I actually feel... while I don't truly think it damaging really not at this point it is in no way uplifting either... with all the googling I have done on disorders since this started I have a terrible unquenchable thirst for it.  So I know I will never be satisfied as I feel there is an answer even if they never let it out and never tell us... when I work my brain is good... I will always seek the answers. 

I hope you are well and thank you for sharing your experience.  I think there is a lot to be found yet.. we are only on the brink of the truth. 

I wish you peace. 

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Thank you btdt, I so appreciate you looking stuff up for me even though you aren't feeling well yourself.  It's over my head but if I their conclusion is right in your first reference it does look like there is some inflammatory response going on...Maybe that's why the herb seems to be working.

 

I hear you about googling too, I still feel there are answers too.  I for some reason never really listened when people said not to look stuff up.  I don't feel it sets me back much to do though like you feel it can be unpleasent.  I have found answers that way too though, plus in severe withdrawal I did know the drugs were the cause of my problems so I tended not to get stuck on ideas like I had a fatal illness.  I can see how people who aren't sure the drugs are to blame would find it scary or even counterproductive.  But for me that wasn't the case at all.

 

Also I looked at what you feel you might have.  That looks scary.  I hope you find your answers, I truly do as you have suffered more than your fair share.

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I should have added, I'm keeping on with the search for something for fatigue as this is now a big problem for me that needs some resolution.

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