I've been on many different ssri's for depression in the last 10 yrs., just started with fatigue in jan. interesting point u make.

The pills could have been your CFS trigger. Most of us probably are predispositioned to get sick because of a gene or something but everyone always constantly has a trigger and it could be anything. My trigger was an allergic reaction. CFS is really complex, this sounds stupid but you could almost compare it to an onions layers. The layers are damages from things in life like viruses, toxins, reactions, pills etc. Everyone has different layers and the more you can peel the layers back the less symptoms you will have. the more layers that grow the more symptoms you will have. Have you read Dr. Sarah Myhills ebook( http://www.drmyhill.co.uk/cfs_book.pdf ) that may have some answers for you. My sister kind of had the same thing happen to her as you did, the only difference was she got in a small car accident and it triggered symptoms then the SSRI's she took for the fatigue that the car accident had triggered made it worse. I am allergic to meds. so I don't have any personal experiences with that at all.

Yeah, I've read Myhills book. Exellent, but I must say, it certainly dosn't make the treatment of CFS simply unless you have a brilliant doctor and lots of money. Yeah, i must say, whether I had CFS coming or not, I'm thoughrougly pissed of that somehting that's supposed to help makes things a thousand things worse. It's very difficult have faith in pdocs after this.

I was on Prozac in 1993. For about 6 months, into 1994.

Desyrel was added because the Prozac wasn't helping me sleep. About 3 months.

I started gaining weight.

I've never been the same.

I have always blamed Prozac for some of my illness. But in 1993, my shrink didn't believe in repetitive muscle injuries, which is what I really had, in addition to delayed caregiver burnout after my husband's accident.

So yes, for me, your post applies.

Hi YesI started on lexapro in april 08 and immediately lost my energy and had very bad mid back aches. These are usually associated with adrenal fatigue. Still battling fatigue and anxiety 7 months after coming off the stuff.
regards
Ginny

How annoying isn't ginny? How are u doing sorting out the adrenal fatigue?

Prior to SSRI's I was OK with a minor depressive condition. After 7 years of SSRI's I was very sick with CFS. It took me 2 years to get of SSRI's. I lost my job, my strength, my endurance and a great part of my health. They were nasty shit. I was a cognative zomby when I was on them. My Dr's said that I have rapid onset post viral CFS (after a mosquito borne infection Barmah forrest virus) and Hep A at the same time. Still to weak to work 5 years later.
Could you please referance your quoats/articles?
Cheers
Al

The quote from the first post was just from http://en.wikipedia.org/wiki/PSSD

this is also from wikipedia
"[edit] Permanent neuropsychological changes
Since the early 80's scientists have used a technique called neonatal clomipramine to produce animals used in depression research. If rats are given the tricyclic antidepressant clomipramine when they are 8-21 days old they will develop behavioural changes in adulthood which resembles depression in humans.[47][48] In 1997 Lundbeck found that treatment with the SSRI LU-10-134-C, which only differs from their product citalopram by two atoms could give similar results as clomipramine.[49] Later it was found that neonatal citalopram and escitalopram makes persistent changes in the serotonergic transmission of the brain resulting in behavioral changes, [50][51] which are reversed by treatment with antidepressants.[52] By treating normal and knockout mice lacking the serotonin transporter with fluoxetine scientists showed that normal emotional reactions in adulthood, like a short latency to escape foot shocks and inclination to explore new environments were dependent on active serotonin transporters during the neonatal period.[53][54]
But when young mice were treated with the SNRI desimipramine they developed to normal adults, which suggests that serotonin and noradrenaline has different effects in the developing brain. For humans, the developmental stage sensitive to SSRI:s corresponds with the last trimester to the first years of life. A study showed that 4-year old children perinatally exposed to SSRI:s behave normally, however the young mice and rats also seems to be normal until they reach puberty and develop their behavioural disturbances.[55][56]
The mechanism is currently unknown, but it seems that early life overstimulation of the 5HT-1 receptor which acts like a thermostat for the serotonin production results in low serotonin production after puberty.[57]
It is believed that sexual dysfunction is caused by an SSRI induced reduction in dopamine. Stimulation of postsynaptic 5-HT2 and 5-HT3 receptors decreases dopamine release from the Substantia Nigra.


this is from a pubmed study discussing SSRI poop out "A mechanism to explain relapse unique to SSRI antidepressant treatment remains uncertain. Recently, McGrath and colleagues[5] proposed that relapse during SSRI maintenance may arise from the SSRI-induced depletion of dopamine in the striatum and limbic forebrain. In a preliminary open study of SSRI augmentation with the dopamine agonist bromocriptine, 6 of 12 (intent-to-treat) patients fully regained remissions from depressive symptoms.

This is from an article called "problems associated with hyprebaric chamber"
Why did the Canucks do so well in the playoffs? First, the playoffs took them away from the hyperbaric chamber for extended periods. Second, the brain under environmental stress from increased positive ions or lack of ions produces hormones and chemicals to deal with this stress. The two main hormones released are melotonin and serotonin. Serotonin is increased and fed into the blood stream. The increased serotonin triggers the release of adrenaline which allows the body to work through the stress. Adrenaline is not quickly renewed as are other chemicals in your body. If a body produces to much serotonin for long duration's, the adrenaline gets used up and the chemical system in the body is unbalanced. This is what was happening with these players. A list of side effects from increasing the serotonin levels in your body for a long period of time are as follows:
Anxiety, nervousness, tremors, sweating, dizziness, lightheadedness, dry mouth, upset or irritated stomach, appetite loss, nausea, vomiting, diarrhea, stomach gas, rash and itching.
Less common side effects include changes in sex drive, impotence, abnormal dreams, difficulty concentrating, acne, hair loss, dry skin, chest pains, allergy, runny nose, bronchitis, abnormal heart rhythms, bleeding, blood pressure changes, headaches, fainting when rising suddenly from a sitting position, bone pain, bursitis, twitching, breast pain, fibrocystic disease of the breast, cystitis, urinary pain, double vision, eye or ear pain, conjunctivitis, anemia, swelling, low blood sugar, and low thyroid activity.
In addition, many other side effects affecting virtually every body system have been reported. They are too numerous to mention

This is from Julia Ross book: The mood cure
"Serotonin is the biochemical counterbalance to your brains natural stimulants, the catechloamines. Raising serotoin levels via SSRI can deplete the levels of these stimulating as much as 60 percent. This can cause low energy, apathy, twitches, tics and sexual dysfunction."

This is http://blog.wired.com/wiredscience/2009/02/antidepressants.html

SSRI antidepressants work by boosting circulating levels of serotonin, a mood-regulating neurotransmitter that also inhibits desire. The drugs also decrease dopamine, a neurotransmitter involved in a wide range of cognitive and behavioral processes, among them desire and arousal. The new research suggests that dopamine may also play a part in romance.
During sex, a cocktail of hormones is released that appears to play important roles in fostering romantic attachment within the brain. Take away sex, and romantic love can dwindle. But this is just part of the problem, say Fisher and University of Virginia psychiatrist James Thomson.
Dopamine also appears central to the neurobiology of romantic love and attachment, conditions that Fisher believes to be affected by but ultimately distinct from sexual love and its effects. She and Thomson say that SSRIs may do more than cause sexual dysfunction: They also suppress romance.
"There are all sorts of unconscious systems in our brain that we use to negotiate romantic love and romantic attraction," said Thomson. "If these drugs cause conscious sexual side effects, we'd argue that there are going to be side effects that are not conscious."
According to Fisher, humans have three distinct but interconnected love-related brain systems: one for sex, another for attachment and another for romantic love. This is still hypothetical nobody knows exactly what love does in the brain but Fisher has been a pioneering researcher on romantic love's neurobiology, and dopamine indeed appears important.
When couples have just fallen in love, the mere sight of the other causes a jump in dopamine-related brain activity. If they manage to stay in love, with the early flush giving way to long-term affection, those brain patterns stay active.
Reduced dopamine levels, however, are an inevitable effect of SSRIs. Reduce dopamine, say Fisher and Thomson, and the possibility of love itself is reduced."

I forget which pubmed study this is from
"The effect of a pharmacologic increase in serotonin concentrations on striatal dopamine (D2) receptor availability has been measured in several studies using positron emission tomography (PET) and the radiotracer [11C]-raclopride as a method for the in vivo imaging of serotonin modulation of striatal dopamine in human subjects. These studies have shown that an acute increase in serotonin concentrations produced a decrease in striatal D2 receptor availability. The current study was undertaken to measure the effects of a more pharmacologically selective serotonergic agent compared to previous studies, the serotonin reuptake inhibitor, citalopram, on striatal D2 receptor availability. Twelve healthy control subjects underwent two PET scans performed on the same day following i.v. administration of saline (Scan 1) and citalopram (Scan 2, 40 mg, i.v.). The [11C]-raclopride data were analyzed with a graphical analysis method using the cerebellum as the input function. Plasma levels of citalopram, cortisol, and prolactin were measured. The citalopram concentrations peaked at the end of infusion (EOI) and remained relatively consistent from 30 min to 3 h postinfusion. An increase in cortisol and prolactin concentrations was observed from the EOI until 60 min after the EOI. A significant decrease in striatal D2 receptor availability was observed after citalopram infusion (-5%), presumably due to an increase in endogenous dopamine concentrations. In summary, i.v. administration of the selective serotonin reuptake inhibitor, citalopram, produced modest reductions in striatal D2 receptor availability, consistent with other human [11C]-raclopride studies using less pharmacologically selective serotonergic agents. Synapse 63:1-6, 2009. 2008 Wiley-Liss, Inc."

Long-Term SSRI Use Tied to Apathy Syndrome
OB/GYN News , May 1, 2001 by Carl Sherman
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HOUSTON -- Depression is a highly cyclic disorder, but not every apparent return of symptoms represents a true recurrence of the disorder.
Late emerging adverse effects, discontinuation phenomena, or drug interacdons may be the true explanation, Dr. Lauren Marangell said at the Psychopharmacology Update 2000 sponsored by Baylor College of Medicine.
Medication adjustments or augmentation strategies can often rectify what seems like a loss of antidepressant effect, said Dr. Marangell, director of clinical psychopharmacology at the university.
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When a patient reports that "the medicine isn't working anymore" after 6-18 months of successful therapy with a selective serotonin reuptake inhibitor (SSRI), the explanation may be the "asthenia/apathy syndrome" rather than a recurrence or simple loss of effect.
In such cases, closer examination will reveal that the symptoms are distinctly different than the patient's prior depression, with the prominent feature often being apathy without sadness, tearfulness, guilt, or hopelessness. "Flattening" of emotions and a loss of motivation are characteristic. In these cases, increasing the SSRI dosage will typically worsen, rather than improve symptoms, Dr. Marangell said.
Although the syndrome has not been studied systematically it appears to develop in 20%-50% of patients on long-term SSRI treatment, and to possibly involve attenuation of dopamine functioning in the frontal cortex, secondary to chronic stimulation of central serotonin neurons.
The addition of a psychostimulant or a switch to a different antidepressant is often effective, she noted.
Dr. Marangell reported an open study of another approach, augmentation with the antipsychotic olanzapine. The trial involved 20 patients who had a diagnosis of major depression, were in remission, had been receiving an SSRI for 3 months or longer, and had elevated scores on scales measuring the "inability to feel" dimension of depression and apathy.
After 8 weeks at the maximal tolerated effective dose, there were significant reductions in apathy and depression scores. The drug was well tolerated except for weight gain--a mean 6.5 pounds.
A return of depressive symptoms also may reflect a drug interaction. For example, fluoxetine, paroxetine, and bupropion are potent inhibitors of the 2D6 isoenzyme of the cytochrome P450 system. If a patient has recently been prescribed a [beta] blocker for hypertension, this inhibition could result in higher than expected levels of that drug, leading to fatigue that resembles depression, Dr. Marangell said.
On the other hand, certain drugs or herbal preparations can induce enzymes that metabolize antidepressants, leading to declines in efficacy. These include carbamazepine, barbiturates (including those contained in certain headache preparations), and St. John's wort.
Inquire carefully about recent changes in medications prescribed by other physicians, as well as self-prescribed herbal remedies, when an antidepressant appears to fail.
An apparent recurrence of depression when drugs are tapered or withdrawn may actually reflect SSRI discontinuation syndrome. Worsened mood, irritability agitation, and fatigue are common manifestations of the syndrome.
A simple way to distinguish this from recurrence is to administer a single dose of the antidepressant; if this resolves symptoms, the drug should be tapered more slowly. If symptoms reappear even when the lowest dose of an SSRI with a short half-life (such as paroxetine) is withdrawn, a dose or two of fluoxetine may provide SSRI coverage long enough to get beyond the discontinuation phase, she said.

This is from a study dissusing ssri sexual side effects
"It is hypothesized that SSRIs affect the sexual response system by raising levels of serotonin. Serotonin, a neurotransmitter, appears to have a negative impact on the desire and arousal phases of the sexual response cycle which consists of four phases including: desire, arousal, orgasm, and resolution. This seemingly occurs through its inhibition of dopamine and norepinephrine, which are other neurotransmitters. Serotonin also appears to exert direct effects on sexual organs by decreasing sensation and by inhibiting nitric oxide. Nitric oxide is thought to be a key player in the sexual pathway as it is thought to relax smooth muscle and blood vessels and therefore allow adequate blood supply to the sexual organs. Overall, it is the interplay of these neurotransmitters that causes antidepressant-induced sexual side effects.

I apologize for my lack of references, I compiled this in a document if I was going to discuss my current situation with my new doc.

ali5stair, I'm sorry to hear that. I wish they weren't overprescribed and more reliable studies were done to document their efficacy and safety.

I was on a high dose of Zoloft with Wellbutrin for over 4 years and know without a doubt that my brain chemistry changed (for the worse) and have never been the same since that time. I was on these ad's from 1991-1996 and it is one of the biggest mistakes I have ever done. I have done a fair amount of research like you and it is very concerning that this has happened to me. I have lost my creativity and inspiration and have had CFS (varying degrees) as well. I want to believe that with the right nutrients etc. I can help my brain do repair but I am not there yet. The other problem I have now is that my liver functions are different. I am very sensitive to chemicals and medications. I have tried to take other ad's since and my body will not tolerate them. I get tons of side affects. Plus I know they won't fix the underlying causes. My depression was not cured-my emotions were just frozen. I am in a daze most of the time and have a ton of memory loss. I feel like I am on auto pilot most of the time. I know my thyroid is out of whack too but the tests show it is normal. I can't go back in time but try to educate others on the pitfalls of anti depressants-especially ssri's. I had no idea what I was doing when they were prescribed to me. I like to say that I was not deficient in anti depressants. I know there are books and diets etc. to improve brain chemistry but it takes so much work to figure it all out. Good luck to you with your recovery from CFS

Interesting read:
http://www.wired.com/magazine/2010/12/ff_dsmv/all/1

I developed CFS twenty five years ago. First symptoms came when I reintroduced birth control pills, after having given birth six months prior. Those pills produced an immediate, horrible reaction. I stopped them, and soon after, succumbed to the same flu that ran through my family of four. They recovered - I never did.

I don't tolerate most pharmaceuticals, and got hives from zoloft, so I can't speak to that. But I think pharmaceuticals can be a contributing factor.

I developed CFS twenty five years ago. First symptoms came when I reintroduced birth control pills, after having given birth six months prior. Those pills produced an immediate, horrible reaction. I stopped them, and soon after, succumbed to the same flu that ran through my family of four. They recovered - I never did.

I don't tolerate most pharmaceuticals, and got hives from zoloft, so I can't speak to that. But I think pharmaceuticals can be a contributing factor.

Dang it, every time I post, it posts twice!