• The Dark Side 💕 Welcome Guest 💕
    Posting Rules Bluelight Rules
    Notable Threads Urgent Hotlines
    Bereavement Mindfulness
    Suicide Support Anger Management
  • TDS Moderators: AlphaMethylPhenyl | paranoid android

Mental Health Coming Off Invega Sustenna (Paliperidone) v.2

Status
Not open for further replies.
@neuroleptique33 my mind is quiet as well. I have no inner speech/monologue. I use to have many thoughts, now its just a single thought. It takes real effort to think.
 
Narshe81 the founder of this thread
28-11-2013 01:02 Report Post
Hi,

I was misdiagnosed with schizophrenia last year and was forced to take Invega Sustenna at 100mg a month for 10 months started back on December 5th 2012. The medication gave me severe anhedonia and rendered me an emotionless zombie who cannot function. I have lost my job and have been on disability ever since. I have lost all of my motivation and willpower to do anything. Even showering seems to be an impossible task. I can no longer feel happy, joy, excited, or pleasure. Things that used to give me pleasure all have stopped working since I started Invega Sustenna. Cigarettes and alcohol no longer have any effects on me since the drug blocks dopamine and serotonin receptors.

My last shot was on August 29th 2013, and I have been off this medication for almost 3 months now. I have yet to feel any improvement at all. This has been the worst experience in my life. The worst form of torture I have ever been through. I won't even wish it upon my worst enemy. The worst part is that weed doesn't even work on me anymore after this medication. No matter how good the buds or how much I smoke, I would feel nothing. Not even a buzz.

I have been trying to find some information about anyone who has successfully came off this drug but I have had no luck. I have read that this drug has a really long half life of 25-49 days, and it takes 5-6 half lives to get rid of a medication, so that's 150-300 days. Does that mean I will have to feel like this for another year at least?

Any information would be greatly appreciated. I am truly desperate.
And this is now 2019 and the final antidote is one stablon in morning and one pacitane in night and am again and again posting this cause I know the tourcher I faced before finding this antidote and I want to help people who really suffer like me and am sure this will happen already few have tried just pacitane and found that to be good for just restlessness and am happy and sure when I post many timess this will come to notice of people
Because I can't sue that company of johnson and johnson or I can't post in facebook or youtube and I have only this valuable medium of blue light
Thnks you have a great year 2019
 
@neuroleptique33 before the shot I was able to think many thoughts at once. Like my mind was full of them. Its been 5 months since my last shot and my mind is still quiet. Its like have to force myself to think. I can respond to people talking to me and carry on a decent conversation. Its like a single thought enters my mind at a time. Takes longer to process information and can't retain it. One of the purposes for invega is to stop the voices in your head which I never suffered from. I've done research to see where thought originates. The ancient Greeks said the pineal gland and modern science states the cerebrum. The cerebrum is the largest section of the brain and is responsible for thinking, senses, and personality (among other things). In short invega is a chemical lobotomy
 
No narshe81 last post was in 2015 and he did not recover very long period cause he took ten injections and no reply from him after that try messaging him he told he felt better after taking street drugs like LSD and other powerful dopamine inhibitors and inhibitors are giving temporary solution
And coming to my picture I took this deadly invega for just three shots and in 2014 feb and march and stopped any antipsychotic
After various research of trying various dopamine agonist my prolactin level was reduced and did not get any results
Tried prescribed dopamine inhibitors like modalert and got temporary results just felt sexual active for few hours and good libido for few hours and did not get permanent results
So was living like this for 2014 to 2017
At last in 2017 June after serious research found that stablon a tricyclic antidepressant cause make gene transcription which is neuroprotective and reverses cerebral damages and neuroplasticity and as a magic with in two days I felt the change and was using it for more than 6 months even started taking large dose as i felt like going back to my teen age my libido increased 200 percent and erectile dysfunction was cured and got interested in love ,dating ,chatting ,gaming ,music ,feeling ,felt am back like human and certain period of taking stablon and pacitane even small dose like just one tablet a day made my high like drunk and so stopped taking any tablet and I found my receptors were back to normal even above normal it's been a year now with out any tablets
 
So I promise you guys never loss your hope it's not permanent it's just like tuning your receptors and temporary fix like adderral which are inhibitors increases dopamine level temporary and even Ritalin is the same I have tried every thing like test piece on my body
 
Do you believe in the healing? Already you can think even if it is little it is well I would like to think I have none… @Nvegasuck
 
Permanent changes occur with stablon and pacitane with dopamine receptor exactly with d2 in mesolimbic pathway and serotonin receptors which is the main target of this invega susttenna
 
I hope that Narshe81 is better since I took only one injection of Risperdal and taken from Risperdal 1 month so 2 months of Risperdal and I really hope that these effect be permanent I can not imagine anything is crazy..
 
Try to understand ya it's not healing once u take invega even a single injection will be above 235mg extended release which stay in muscles for months together and what happens is it reaches saturation point and it changes permanent your dopamine and serotonin system and you need a boost to tune your level of secretion which can be done by stablon and pacitane
 
@Neuroleptique33 Narshe actually recovered, but he realised it after getting another injection so he was back to stage one. That's what I remember reading. Don't worry too much Neuroleptique33 you are gonna be fine
 
Tianeptine (Stablon, Coaxil, Tatinol) is a neuroprotective antidepressant that reverses the neuronal damage and lasting misery caused by chronic, uncontrolled stress. Tianeptine acts both as a non-sedating anti-anxiety agent and a non-stimulating mood-brightener. Uniquely in clinical medicine, tianeptine acts as a selective serotonin reuptake enhancer. Its puzzling efficacy as an antidepressant illustrates how little modern psychiatric medicine really understands about mind, mood and depression.

A breakthrough in tianeptine research was announced in July 2014 with the unexpected discovery that tianeptine is a full agonist at the mu and delta opioid receptors with negligible effect at the kappa opioid receptors. Selective mu opioid agonists in the brain's "hedonic hotspots" typically induce euphoria. Selective kappa agonists typically induce dysphoria. The role of central delta opioid receptors is poorly understood. Dual activation of the mu and, less potently, delta opioid receptors may be critical to tianeptine's mood-brightening and anxiolytic effect - a therapeutic action seemingly unaccompanied by the physiological tolerance and dependence that have plagued traditional opioids. All previous research into tianeptine may need to be re-evaluated in this light. Neonatal Abstinence Syndrome following heavy use of tianeptine during pregnancy has been reported. The recently popular sulfate salt (tianeptine sulphate) is less readily absorbed and excreted from the body than the sodium salt, allowing one-per-day dosing, smoother plasma concentrations, and minimal risk of abuse. More research is urgently needed.

An inverse correlation exists between the suicide rate and dietary intake of the essential amino acid l-tryptophan, the rate-limiting precursor of serotonin synthesis. The widely prescribed selective serotonin reuptake inhibitors [i.e. the SSRIs fluoxetine (Prozac), sertraline (Zoloft), fluvoxamine (Luvox), paroxetine (Paxil) and citalopram (Celexa)] block the reuptake of the neurotransmitter serotonin into the presynaptic nerve cells by interfering with the serotonin transporter. They thereby increase the availability of serotonin in the synapse. SSRIs are marketed primarily as antidepressants. They are prescribed for a host of off-label indications too. In contrast to SSRIs, tianeptine facilitates the reuptake of serotonin into serotonergic terminals both in the cortex and hippocampus - confounding simplistic "low serotonin" theories of depression. Tianeptine lacks any significant activity at monoamine transporters or neurotransmitter receptors. How it actually accelerates serotonin reuptake, both acutely and chronically, is unclear. Like other contemporary antidepressants, its therapeutic action presumably depends on downstream adaptations both between and within neurons occurring over a period of several weeks.
 
y patent-protected.

How does tianeptine/Stablon work? No one really knows. So the story below will soon be superseded. Tianeptine is neuroprotective via multiple neurochemical and cellular mechanisms. When an organism is under stress, or perceives itself under stress, the hypothalamus secretes corticotropin-releasing hormone/factor (CRH/CRF). CRH/CRF in turn increases secretion of adrenocorticotrophic hormone (ACTH) from the anterior pituitary. ACTH in turn stimulates the release of glucocorticoids from the adrenal cortex. Persistent, uncontrolled physical and psychosocial stress causes excess cortisol secretion from the adrenal glands. Excess cortisol causes dendritic shrinkage in the hippocampus and a contrasting growth of dendrites in the lateral amygdala. These stress-induced changes tend to lower mood; they can cause clinical depression in the genetically vulnerable. Current evidence suggests that tianeptine acts to prevent and even reverse stress-induced neural damage, promoting both neuronal survival and synaptic plasticity. Sustained use of tianeptine tends to "normalise" the hypothalamic-pituitary-adrenal (HPA) system. Tianeptine reduces basal and stress-evoked activity of the HPA, helping its users cope in a stressful environment. Treatment with tianeptine inhibits corticosterone-induced gene transcription. Stress-induced increases in plasma ACTH, and corticosterone levels are diminished. So too is basal activity of corticotropin-releasing factor (CRF) neurons and their sensitivity to stress. Prolonged tianeptine use also reduces some forms of stress-induced apoptosis ("programmed cell-death"), notably in the temporal cortex and dentate gyrus of the hippocampus. At the molecular level, tianeptine exerts profound effects on the glutamate system. The amino acid glutamate serves as the main excitatory neurotransmitter in the brain. Its excitatory action is mediated by via multiple receptor subtypes. The three main subtypes of glutamate-gated ion channel are kainate, ampa, and N-methyl-D-aspartate (NMDA). Tianeptine prevents overstimulation of AMPA/kainate type glutamate receptors in the hippocampus that regulate Ca2+ entry into the nerve cell; excess Ca2+ entry into nerve cells is toxic. Tianeptine also modulates the NMDA glutamate receptors. NMDA receptors for glutamate play a critical role in mediating the functional and intracellular effects of stress. Tianeptine reportedly targets the phosphorylation-state of glutamate receptors in the hippocampus, "normalising" stress-induced changes in the amplitude ratio NMDA glutamate receptor to AMPA/kainate glutamate receptor-mediated excitatory post-synaptic currents. Selective glutamate receptor antagonists, including sub-anaesthetic doses of the dissociative anaesthetic ketamine, can act as analgesics and neuroprotective antidepressants, despite dose-limiting side-effects. Their mind-altering properties deter wider clinical psychiatric use. Tianeptine, on the other hand, is an analgesic and antidepressant that lacks psychotomimetic side-effects at any sensible dose.
 
@neuroleptique33 truthfully some days I believe ill be healed. I think the brain is capable of healing but very slowly. Other days I have no hope, that ill never get my thoughts back that this drug caused serious brain damage. I just keep hoping one day ill wake up and ill just be thinking. I just try to teach my mind (I could be better about it) I luckily have a friend who loves to talk, I feel that has helped because it forces me to think. Reading, even though retaining the information is hard. Documentaries. Instead of meditating to quiet the mind I meditate to listen to the mind. I do an affirmation while I mediate. I just want to keep the mind as active as possible.
 
Unlike SSRIs and other "serotonergic" antidepressants, tianeptine does not dampen libido or sexual performance. Indeed sexual function may even be enhanced. Depression, dysthymia and the spectrum of "subclinical" depressive disorders damage not just millions of afflicted individuals, but their partners and wider circle of friends and family. Unfortunately, no controlled studies have been done on the effects of existing psychotherapeutic drug treatments on the user’s personal relationships. Thus SSRIs have helped save many intimate relationships, yet they have also broken them. For SSRIs can diminish both the intensity of being in love and the ardour with which to express it. One makeshift option is to correct SSRI-induced sexual and romantic deficits with cautious polypharmacy. Authentic aphrodisiacs like Palatin's melanocortin agonist PT-141 (bremelanotide) are already circulating in the scientific counterculture and beyond. A veritable cultural revolution may be brewing. Yet the likelihood of ubiquitous recreational use of inhalable sex-drugs may discourage an FDA product license.
 
Unlike its pro-sexual cousin amineptine, tianeptine does not significantly inhibit the synaptic reuptake of dopamine when taken at normal doses. But tianeptine does acutely increase extracellular dopamine concentration in the nucleus accumbens and, at higher doses, in the frontal cortex. The functional responsiveness of dopamine D2/D3 receptors is also enhanced. "Supra-therapeutic" doses of tianeptine are mildly stimulating and noticeably mood-lifting. But tianeptine is (almost) without a tendency to uncontrolled dose-escalation; rare chronic high-dosage tianeptine use is pursued for a gentle stimulant effect that is virtually absent at approved and divided doses. High-dose tianeptine also feels smoother than high-dose amineptine. In common with the SSRIs, tianeptine is (relatively) safe even in massive overdose. It's certainly less hazardous than its cardiotoxic tricyclic relatives.

Tianeptine inhibits activity of the enzyme nitric oxide synthase (NOS) in the hippocampus. This is an important subcellular signalling system for the glutamate-NMDA receptor. NOS inhibitors have distinct antidepressant properties. NOS levels are higher in depressives than "euthymic" normals. The effects of tianeptine on the glutamate-NO pathway explain the improved cardiovascular status of tianeptine-using patients with ischaemic heart disease. There is a poorly understood association between coronary heart disease and depression; disturbances in nitric oxide production may play a role in both.
 
Status
Not open for further replies.
Top