Psycho-Babble Medication | about biological treatments | Framed
This thread | Show all | Post follow-up | Start new thread | List of forums | Search | FAQ

Re: LDN Low Dose Naltrexone Questions

Posted by casse on January 9, 2010, at 13:39:27

In reply to Re: LDN Low Dose Naltrexone Questions, posted by Elroy on January 8, 2010, at 16:56:18

Wow, what an ordeal you've been through!

The antidepressant I just started taking is supposed to help with damage to the HPA axis caused by chronic stress. With your chemistry background and gift for analogy, I wonder if you could simplify this. This is an excerpt from THE GOOD DRUG GUIDE

http://www.tianeptine.com/

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 So the story below will soon be superseded.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.


I've been using tianeptine for a week now, and have had the most remarkable relief in some extremely distressing symptoms that my psychonaut attributes to anxiety: stomache aches, choking feeling, pelvic pressure, and feeling like my chest is being squeezed, cold hands and feet, loss of focus, fatigue, and muscle tension and pain. I have had strong suspicion that this is a physical problem and not a mental one, and I get minimal relief from the muscle relaxant tizanadine.

It seems my GYN is in agreement. She urged me to ramp up the tianeptine to full dose asap and gave me some ativan for short term use to help in case it made me too nervous at first. She also refered me to a Gastrointerologist as she believes that's the source of the problem. What's interesting is, when I take the tianeptine, I get almost complete relief of the symptoms, but they return as the drug is metabolized. It has a short half-life and must be taken throughout the day to maintain levels. I wonder, if my problem stems from my GI tract, why is the tianeptine helping the symptoms?

I respect your input, the sooner I get this resolved, the sooner I can get on with LDN.

Casse


Share
Tweet  

Thread

 

Post a new follow-up

Your message only Include above post


Notify the administrators

They will then review this post with the posting guidelines in mind.

To contact them about something other than this post, please use this form instead.

 

Start a new thread

 
Google
dr-bob.org www
Search options and examples
[amazon] for
in

This thread | Show all | Post follow-up | Start new thread | FAQ
Psycho-Babble Medication | Framed

poster:casse thread:919880
URL: http://www.dr-bob.org/babble/20100103/msgs/933035.html