I feel like "me" again, and it was immediately after I stopped Fetzima. The first day was like turning on a light switch. I've been on Cymbalta for 2 days and there is no more anxiety, frustration or hypomania (racing thoughts, snapping at people, etc)
I'm sorry if I sound like a robot or computer, but I've learned that I have to understand what my medications are intended to help. If you're like me, you started taking your meds to feel better and if it worked, you were happy. When I start to feel crappy, I want to know what happened. I hope this helps anybody who tried Fetzima and didn't like the feeling of being on the brink of losing your temper and patience during every moment that you were awake.
This article was a good start for me: http://www.pharmathe...-for-depression
In July of 2013, the FDA approved a new serotonin norepinephrine reuptake inhibitor (SNRI) Fetzima (levomilnacipran) for major depressive disorder in adults only. The efficacy of Fetzima at once-daily doses of 40-120mg was established in three randomized, placebo-controlled studies in adults with MDD.
Fetzima is essentially an isomer, or put more simply, a clone of the SNRI Savella, which is approved for the treatment of fibromyalgia. The interesting thing is that Fetzima is not approved for fibromyalgia and Savella is not approved for depression. Go figure. Round up the usual suspects when it comes to the side effects of Fetzima – nausea, heart rate increase, palpitations, erectile dysfunction and other associated SNRI side effects.
There’s nothing new or novel here. Just another drug – in this case Savella – that has undergone a makeover to be marketed for depression.
The snail’s pace of neuroscience continues to hamper pharmaceutical companies in their quest to develop truly novel agents. What we don’t need is yet another SNRI poised to fuel oppositional tolerance, which places the brain in a fighting position to counter the effects of artificial serotonin and norepinephrine manipulation rendered by these antidepressants.
The words that I highlighted in red caught my eye, so I kept looking for info. I had an idea of what "oppositional tolerance" meant because my Doctor had explained it to me as "Fetzima creates a serontonin and norepinephrine imbalance which favors norepinephrine not serotontin. "
After I searched, I found an article which explained oppostional toloerance in more clinical terms and it may explain why some of us started becoming anxious and snapping at people. Our brains were out of balance and the serontonin and norepinephrine imbalance made us feel yucky.
Fetzima caused "brain-fighting" that Dr Giovanni Fave described in 1994 as "oppositional tolerance".
When you read these notes, remember that Fetzima lowers serontonin and increases norepinephrine levels in the brain:
1. As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled.
A. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle.
B. Epinephrine and norepinephrine, are also called adrenaline and noradrenaline, two separate but related hormones secreted by the medulla of the adrenal glands.
2. Serotonin is a hormone found in the digestive tract, the central nervous system, blood platelets and the pineal gland (deep at the center of the brain).
It is also known as 5-hydroxytryptamine, which is often abbreviated to 5-HT.
A. Serotonin cannot cross the blood-brain barrier. Therefore serotonin that is used inside the brain must be produced within it.
B. Serotonin's effects on a range of functions tend to be inhibitory. In other words, it reduces appetite, sexual behavior, and suppresses pain perception.
C. According to researchers at the absence of serotonin has been associated with greater aggressive behavior. They say that serotonin levels have been correlated with higher levels of irritability, impulsivity, aggression, disordered eating, and sleeping problems.
I think "2C" sums up why some of us didn't feel well while trying to use Fetzima. I truly hope it helps some of you.
This is the link to the article which describes how Dr. Giovanni Fava and other practitioners had observed that antidepressants seemed to worsen the long-term course of depression.
Dr Fava used the term "oppositional tolerance" for what was caused by medications. I'm going to talk to my Doctor about the last 2 sentences in the excerpt below.
For me, what it means is that the longer I stay on an SSRI or SSNRI, the less serontonin my brain will produce. It explains why I was OK on 30 mg of Cymbalta for 3 years and then had to go to 60 mg of Cymbalta for the past 2 years. It also explains why so many people become resistant to SSRIs and SSNRIs.
It was in 1994 that Italian psychiatrist Giovanni Fava, editor of Psychotherapy and Psychosomatics, urged the field to directly confront this possibility.
In subsequent papers, GIovanni Fava set forth a biological explanation for why this may be so. Psychiatric drugs perturb neurotransmitter pathways in the brain and in response to that perturbation, the brain undergoes a series of compensatory adaptations in an effort to maintain normal functioning of those systems. In scientific terms, the brain is trying restore its “homeostatic equilibrium.” Fava has dubbed this compensatory response to a psychiatric drug “oppositional tolerance.”
For instance, a selective serontonin reuptake inhibitor (SSRI) blocks the normal reuptake of serotonin from the synaptic cleft, which is the tiny gap between neurons. Serotonin now stays in the cleft longer than normal, and feedback mechanisms immediately kick into gear. The presynaptic neurons begin putting out less serotonin than usual, while the postsynaptic neurons—the neurons receiving the message—decrease the density of their receptors for serotonin. The drug is acting as an accelerator of serotonergic activity; the brain responds by putting down the brake.
Edited by Sayonara2013, 31 January 2014 - 06:17 PM.