Can anyone make sense of this to explain to a layperson?

[[Lo...]]

I think cs123 has indicated he will not continue on this thread, and I suspect that for the most part that will end my participation as well.

 

It's true that CS123 has been the backbone of this thread.  It's benefited from contributions from people like YOU though too, and others.  Perhaps it won't be so active but I hope that when postings happen from time to time we can all check in and put our two cents worth forward.

 

For example.  As usual, the ongoing research and consideration of options led me to consider trying N-acetyl cysteine.  Why?  Well, it upregulates glutamate transporters and I have concerns about extrasynaptic glutamate concentrations.  Also, I'd like to find ways to get down on my gabapentin because I am stalled, stuck, and struggling with it even though my dose is 'low'.  So, over the last 4 days I have been been taking NAC at 600mg BID until yesterday whereupon I took it only during the afternoon in 1 dose.

 

About an hour to an hour and a half after taking NAC, I experienced a significant increase in my burning pain sensations.  By the time I took my evening dose the pain had settled a little bit but again increased afterward.  This pattern continued over the last few days consistently.  Yesterday, I took the dose in the afternoon to see if the pattern followed NAC dosing and sure enough, an hour and 15 minutes later, my burning pain increased. 

 

While this sucks, it is fascinating to me given that NAC  research  has found support for it's analgesic capability in neuropathic pain. So, just curious if others have any opinions or experiences with NAC that weren't positive.  I'm really disappointed as I was hoping to reduce extrasynaptic glutamate with it as NAC modulates glutamate transporters and the cystine / glutamate antiporter system. (Interestingly, it is purported to have a role in the chelation of toxins.  I was exposed to a high amount of toxins, especially in childhood, up until the age of 30.  Anyway, that's a bit outside the scope of this forum).  Just curious about others.  Did anyone have problems to begin with and then they resolved with NAC?  Or any other experiences?

 

-RST

 

Yes. True. It has been a very, very beneficial thread. I'm sad to see cs123 leave. He has poured in a ton of really excellent work in this, and I have recommended this thread to many as a really good source of quality information.

 

As far as NAC goes, no I have not taken it. The one thing I keep trying to remember about Gabapentin in general is that it has nonlinera pharmacokinetics and the bioavailability of it is not stellar.

 

https://olh.ie/wp-content/uploads/2014/09/What-conversion-ratio-is-recommended-between-pregabalin-and-gabapentin.pdf

 

Background

Although gabapentin and pregabalin were originally developed as antiepileptic drugs both

are also licensed for the treatment of neuropathic pain.1,2

The mechanism of action is similar for pregabalin and gabapentin. Both drugs bind to the

α2δ subunit of voltage-gated calcium channels in the central nervous system.

1,2,3,4

Gabapentin has nonlinear pharmacokinetics, meaning careful titration of dose is required,

whereas pregabalin possesses linear pharmacokinetics, which means dosing regimens are

more straightforward.3,4

 

Based on these maximum doses, Toth et al, assumed that pregabalin is six times more

potent than gabapentin.

7 However this assumption has not been proven by robust evidence.

Toth et al carried out a cohort study of 116 patients with peripheral neuropathy and

neuropathic pain assessed the outcomes of switching from pregabalin to gabapentin

 

https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020235s041,020882s028,021129s027lbl.pdf

Oral Bioavailability: Gabapentin bioavailability is not dose proportional; i.e., as dose is

increased, bioavailability decreases. Bioavailability of gabapentin is approximately 60%, 47%,

34%, 33%, and 27% following 900, 1200, 2400, 3600, and 4800 mg/day given in 3 divided

doses, respectively. Food has only a slight effect on the rate and extent of absorption of

gabapentin (14% increase in AUC and Cmax).

 

 

Gabapentin is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but

it does not modify GABAA or GABAB radioligand binding, it is not converted metabolically into

GABA or a GABA agonist, and it is not an inhibitor of GABA uptake or degradation.

Gabapentin was tested in radioligand binding assays at concentrations up to 100 µM and did not

exhibit affinity for a number of other common receptor sites, including benzodiazepine,

glutamate, N-methyl-D-aspartate (NMDA), quisqualate, kainate, strychnine-insensitive or

strychnine-sensitive glycine, alpha 1, alpha 2, or beta adrenergic, adenosine A1 or A2,

cholinergic muscarinic or nicotinic, dopamine D1 or D2, histamine H1, serotonin S1 or S2,

opiate mu, delta or kappa, cannabinoid 1, voltage-sensitive calcium channel sites labeled with

nitrendipine or diltiazem, or at voltage-sensitive sodium channel sites labeled with

batrachotoxinin A 20-alpha-benzoate. Furthermore, gabapentin did not alter the cellular uptake

of dopamine, noradrenaline, or serotonin.

[[Tr...]]

Thank you for the informative and thoughtful replies Liberty and Lorazepamfree2015

[[Lo...]]

I think that the first study that showed a danger of suddenly stopping benzodazepines was the Leo Hollister study done in 1961. I recall prof. Malcom Lader referring to that study in one of the interviews.

 

The thing is that these were doses that were far above the therapeutic levels, and it became clear that librium should not be discontinued abruptly.

https://link.springer.com/article/10.1007/BF00429621

 

Also:

https://books.google.com/books?id=sgkXBQAAQBAJ&pg=PA141&lpg=PA141&dq=leo+hollister+librium+study&source=bl&ots=R-8gee-c-X&sig=RvGRzSg7Ek4RhnJsCbmt3a78AhM&hl=en&sa=X&ved=2ahUKEwiw_f3krb7eAhU0GTQIHZ5IDjAQ6AEwDnoECAgQAQ#v=onepage&q=leo%20hollister%20librium%20study&f=false

[[Lo...]]

Bump.

[[li...]]

A couple points I have to deal with:

 

- damage to the body outside the CNS that does not conform to formal organ or illness pathology. In a way that affects the functioning of the CNS, impairs normal physical functioning and causes physical distress. Cause 'medical treatment' without 'informed consent' and incredible sloppiness. I did mention that this 'doc' factually blocked me from stopping with clonazepam ?

 

- damaged GABAA receptors.

 

- altered GPCRs, in particular altered serotonergic and cholinergic systems. Partly by the clonazepam, partly by health issues/physical stress.

 

- some other various forms of damage 'neural pathways'/'circuit level'. Up to a point, altered neural pathways. Neurogenesis ?

 

- complete absence of competent or service oriented doctors.

 

It's fun, isn't it ? Note: I've taken this drug for 10  years.

 

 

[[Re...]]

A couple points I have to deal with:

 

- damage to the body outside the CNS that does not conform to formal organ or illness pathology. In a way that affects the functioning of the CNS, impairs normal physical functioning and causes physical distress. Cause 'medical treatment' without 'informed consent' and incredible sloppiness.

 

- damaged GABAA receptors.

 

- altered GPCRs, in particular altered serotonergic and cholinergic systems. Partly by the clonazepam, partly by health issues/physical stress.

 

- some other various forms of damage 'neural pathways'/'circuit level'. Up to a point, altered neural pathways. Neurogenesis ?

 

- complete absence of competent or service oriented doctors.

 

It's fun, isn't it ?

 

Thanks for those links, lorazepamFree!  I am going to get around to reading them as soon as I can.

 

LIBERTY:  There are those issues that are outside just benzo problems.  I was also damaged to some degree prior to benzos although I didn't recognize it at the time.  For me, I know I must have a fairly high toxic load given the environment I was raised in and some of the work that I have done over the years, very often without personal protective equipment.  Interestingly, when I took NAC recently, I had a strong negative reaction to it.  My symptoms, especially burning pain became more intense for about 6 or 7 hours thereafter and then started to resolve.  I found this so strange.  I know I mentioned this in an earlier post but some information seems to suggest that NAC may also have a role in chelation.  Perhaps I was feeling some effect of the toxic load being liberated from tissues.  As I've never done any toxin removal therapy, I don't know what the sensation is.  Perhaps I'll try to detox with some dmsa and see what the sensation is!!!

 

Just not now..... I feel like crap!

 

-RST

[[Tr...]]

A couple points I have to deal with:

 

- damage to the body outside the CNS that does not conform to formal organ or illness pathology. In a way that affects the functioning of the CNS, impairs normal physical functioning and causes physical distress. Cause 'medical treatment' without 'informed consent' and incredible sloppiness. I did mention that this 'doc' factually blocked me from stopping with clonazepam ?

 

- damaged GABAA receptors.

 

- altered GPCRs, in particular altered serotonergic and cholinergic systems. Partly by the clonazepam, partly by health issues/physical stress.

 

- some other various forms of damage 'neural pathways'/'circuit level'. Up to a point, altered neural pathways. Neurogenesis ?

 

- complete absence of competent or service oriented doctors.

 

It's fun, isn't it ? Note: I've taken this drug for 10  years.

 

liberty

 

You mention GPCRs being impaired. What exactly do you mean by this?

 

Could seretoninic injury result from AD withdrawal cause this? Could the reaction we’ve had to anticholergenics cause this too?

 

Im a newbie here. So much to wrap my benzo-damaged mind around

 

 

[[Lo...]]

A couple points I have to deal with:

 

- damage to the body outside the CNS that does not conform to formal organ or illness pathology. In a way that affects the functioning of the CNS, impairs normal physical functioning and causes physical distress. Cause 'medical treatment' without 'informed consent' and incredible sloppiness. I did mention that this 'doc' factually blocked me from stopping with clonazepam ?

 

- damaged GABAA receptors.

 

- altered GPCRs, in particular altered serotonergic and cholinergic systems. Partly by the clonazepam, partly by health issues/physical stress.

 

- some other various forms of damage 'neural pathways'/'circuit level'. Up to a point, altered neural pathways. Neurogenesis ?

 

- complete absence of competent or service oriented doctors.

 

It's fun, isn't it ? Note: I've taken this drug for 10  years.

 

liberty

 

You mention GPCRs being impaired. What exactly do you mean by this?

 

Could seretoninic injury result from AD withdrawal cause this? Could the reaction we’ve had to anticholergenics cause this too?

 

Im a newbie here. So much to wrap my benzo-damaged mind around

 

I have not heard of GPCRs before, and not exactly sure what he meant, but this is what I discovered:

 

https://www.nature.com/scitable/topicpage/gpcr-14047471

G-protein-coupled receptors (GPCRs) are the largest and most diverse group of membrane receptors in eukaryotes. These cell surface receptors act like an inbox for messages in the form of light energy, peptides, lipids, sugars, and proteins. Such messages inform cells about the presence or absence of life-sustaining light or nutrients in their environment, or they convey information sent by other cells.

 

GPCRs play a role in an incredible array of functions in the human body, and increased understanding of these receptors has greatly affected modern medicine. In fact, researchers estimate that between one-third and one-half of all marketed drugs act by binding to GPCRs.

 

https://www.hindawi.com/journals/aps/2012/416864/

Figure 3: Functional crosstalk between G-protein coupled receptors (GPCRs) (which are present in the serotonin, dopamine, acetylcholine system) and GABAA receptors is facilitated through multiple protein kinases and scaffold proteins. GABAA receptor β and γ2 subunits are phosphorylated (P) by PKA and PKC upon the activation of individual GPCRs for dopamine and serotonin. PKA phosphorylation of GABAA receptor β1 and β3 subunits is dependent upon AKAP150/79, which directly interacts with these receptor subunits. AKAP150/79 also binds inactive PKA composed of regulatory ® and catalytic © subunits. In addition, PKC phosphorylates the receptor β1–3 and γ2 subunits. Upon the activation of the appropriate GPCR, PKC-mediated phosphorylation is facilitated by the direct (but independent) interaction of the receptor for activated C kinase (RACK-1) and the β isoform of PKC with the GABAA receptor β1–3 subunits. RACK-1 facilitates functional regulation of GABAA receptors by controlling the activity of PKC associated with these proteins. The GABAA receptor γ2 subunit is also phosphorylated by Src, and this kinase is capable of binding to receptor β and γ2 subunits. Finally, the functional effects of phosphorylation are diverse and range from inhibitions to enhancements of GABAA receptor activity, dependent upon the receptor subunit composition. Reprinted by permission from Elsevier, reprinted from [95].

 

 

[[Re...]]

https://www.hindawi.com/journals/aps/2012/416864/

Figure 3: Functional crosstalk between G-protein coupled receptors (GPCRs) (which are present in the serotonin, dopamine, acetylcholine system) and GABAA receptors is facilitated through multiple protein kinases and scaffold proteins. GABAA receptor β and γ2 subunits are phosphorylated (P) by PKA and PKC upon the activation of individual GPCRs for dopamine and serotonin. PKA phosphorylation of GABAA receptor β1 and β3 subunits is dependent upon AKAP150/79, which directly interacts with these receptor subunits. AKAP150/79 also binds inactive PKA composed of regulatory ® and catalytic © subunits. In addition, PKC phosphorylates the receptor β1–3 and γ2 subunits. Upon the activation of the appropriate GPCR, PKC-mediated phosphorylation is facilitated by the direct (but independent) interaction of the receptor for activated C kinase (RACK-1) and the β isoform of PKC with the GABAA receptor β1–3 subunits. RACK-1 facilitates functional regulation of GABAA receptors by controlling the activity of PKC associated with these proteins. The GABAA receptor γ2 subunit is also phosphorylated by Src, and this kinase is capable of binding to receptor β and γ2 subunits. Finally, the functional effects of phosphorylation are diverse and range from inhibitions to enhancements of GABAA receptor activity, dependent upon the receptor subunit composition. Reprinted by permission from Elsevier, reprinted from [95].

 

Now you're hitting the nuts and bolts of this stuff, LorazepamFree.  Because of my inadvertent damage due to physical stress post benzo and during gabapentin tapering,  I have done some research on what happens during exercise. Researchers have discovered over 1000 individual changes that occur in muscle as a result of exercise.  Can you believe it, 1000 different metabolic activities within muscle tissue are modulated during exercise.  It's mind boggling.  It makes sense that GPCR's are critical here.  If we think about it, gene proteins are are set into motion when their receptors are activated and when that happens they start influencing transcription factors that influence gene expression.  So, downregulation of our alpha1 subunits is likely due to some phosphylation induced by a GPCR that is influenced by benzodiazepines directly, or a secondary process influenced by the increase in gabba receptor activation.  If we could get control over some of the phosphorylation processes with small molecules (drugs), there might be a place to cause modulation leading toward healing.  There is a lot to think about in these areas. 

 

The website for Selleck chemicals has interesting signalling pathway maps.  For example, if you go to this webpage:  https://www.selleckchem.com/products/Flumazenil.html  you can scroll down a little on the right side of the page and click on a gaba receptor signaling pathway map.  Check out the processes that are at work.  Now, consider overlaying that map on top of a hundred other maps for different pathways, such as the estrogen/progesterone pathway map. https://www.selleckchem.com/products/Estriol(Oestriol).html  Now, the interaction and complexity goes up and up and up with the more complicated the cell.  No wonder it takes a while for our circuits to rewire when we mess with them!!!  These two pathway maps show something interesting.  Both the gabba pathway and the estrogen/progesterone pathway have processes involving cAMP, (cyclic AMP).  cAMP is can be modulated by forskalin.  OK, let's pretend there is an argument for increased cAMP activity as a way to reduce BZD withdrawal.  So, we all take forskalin.  Yay, BZD has been reduced.  OK, but now we've also messed with the estrogen/progesterone pathway and suddenly we have a major issue with severely elevated testosterone levels!!!  This is why so many therapies that seem promising at first from preclinical data and in vitro studies end up disappointing, ineffective or produce too many side effects.  As science advances and pharmacological target specificity becomes more refined, very subtle and elegant manipulation of biochemistry will be the norm.  Too bad it's not available right now.

 

-RST

 

[[Tr...]]

RST,

 

Did exercise complicate your recovery?

[[Re...]]

RST,

 

Did exercise complicate your recovery?

 

Yes, I am afraid to say that physical stress (hard work or recreational exercise) caused me to have problems.  Progressively, I had less and less resilience.  I didn't draw the correlation because I was only focused on gabapentin tapering and that my problems were a function of that taper.  So, I stressed my body multiple times through physical activity which was effectively like inducing setbacks for myself.  Sadly I induced several such setbacks before I realized the critical role excessive exercise played in my progression to date.  Had I understood what was happening I think I would have been able to manage the taper of gabapentin without too much difficulty and been a good way along to recovery by now.  Unfortunately, I'm in a pretty rough spot and still taking gabapentin. 

 

Exercise is important for our overall health, of course.  It's just that it can also destabilize our neural systems if too intense.  Judging what intensity is not going to cause damage is the trick.  The key is to keep it low, and not intense until you see how you react.  Then, you can slowly increase it over time incrementally.  That is the safe method.  Others just go for it and have no problems.  Some go for it and crash hard and end up being in a setback. 

 

-RST

[[li...]]

LPF,

 

That's some complicated stuff. you know, I would just check wiki ...

 

In my mind it particulary refers to the receptors for serotonin (have you seen the list ? https://en.wikipedia.org/wiki/5-HT2_receptor etc.) and acetylcholine. Of course, also glutamate. Phrase 'neuromodulator'.

 

I think it's really all in this thread, feel free to read up on stuff ...

 

RST,

'Now you're hitting the nuts and bolts of this stuff, LorazepamFree.  Because of my inadvertent damage due to physical stress post benzo and during gabapentin tapering,  I have done some research on what happens during exercise. Researchers have discovered over 1000 individual changes that occur in muscle as a result of exercise. Can you believe it, 1000 different metabolic activities within muscle tissue are modulated during exercise.  It's mind boggling.  It makes sense that GPCR's are critical here.  If we think about it, gene proteins are are set into motion when their receptors are activated and when that happens they start influencing transcription factors that influence gene expression.  So, downregulation of our alpha1 subunits is likely due to some phosphylation induced by a GPCR that is influenced by benzodiazepines directly, or a secondary process influenced by the increase in gabba receptor activation.  If we could get control over some of the phosphorylation processes with small molecules (drugs), there might be a place to cause modulation leading toward healing.  There is a lot to think about in these areas.  ' Well, (have not verified the information) that would suggest exercise is not so good ... Even more complicated with clonazepam.

 

'So, downregulation of our alpha1 subunits is likely due to some phosphylation induced by a GPCR that is influenced by benzodiazepines directly' Honestly, I'm not sure if that's correct. I was thinking that direct exposure of the alpha 1 subunits by a benzo would downregulate the receptor. I have not studied that in detail.

 

GCPRs affect GABAA receptors. It's  all in the thread.

 

Anyway, it's none of my business. But I think you were at one point considering quitting your job, selling your house for the recovery ? (mentioned in the thread) How did that work out ? Maybe I'm confusing you with someone else.

 

 

[[Re...]]

'So, downregulation of our alpha1 subunits is likely due to some phosphylation induced by a GPCR that is influenced by benzodiazepines directly' Honestly, I'm not sure if that's correct. I was thinking that direct exposure of the alpha 1 subunits by a benzo would downregulate the receptor. I have not studied that in detail.

 

Thanks for pointing this out, Liberty.  I didn't articulate it well at all.  What I meant was that during the process when a benzo binds to the gaba a receptor there is a direct downstream effect that results in one of the myriad of GPRC's to start phosphorylation of the alpha-1 subunit out of the membrane to be replaced with a subunit that is less sensitive to the gaba neurotransmitter.  So, yes,  the subunit is downregulated by the benzo binds to the receptor, but the mechanism is via phosphorylation, that probably involves GPCR's.

 

I haven't been able to quit or sell my house.  My wife isn't working now because our son is ill.  As much as I am struggling I've kept my illness from him for almost 20 months as I don't want him to have more stress.  So, now I have to keep going to work.  I could really use a lottery win about now, honestly!!!!   

 

-RST

[[li...]]

RST, only by the GCPR ?

 

I would have expected a direct effect as well. By exposure of the GABAA receptor to the benzo.

 

RST,

 

'I haven't been able to quit or sell my house.  My wife isn't working now because our son is ill.  As much as I am struggling I've kept my illness from him for almost 20 months as I don't want him to have more stress.  So, now I have to keep going to work.  I could really use a lottery win about now, honestly!!!!    '

 

I'm sorry to hear that. Best wishes. I know how hard any additional stress can be.

 

[[Re...]]

Hi Liberty

 

I'm not saying exclusively by GCPR's.  It is but one process.  Another part of the puzzle is the modulation of VGCC's.  Professor Tietz showed that chronic BZD exposure significantly reduces the action potential voltage necessary to activate the high voltage L-type VGCC's.  Those channels then allow a significant increase in intracellular calcium levels and subsequent neuronal excitability.  I think this is why gabapentin was a miracle for me in the beginning but isn't any longer due to tolerance to it. 

 

RST

[[Lo...]]

Hi Liberty

 

I'm not saying exclusively by GCPR's.  It is but one process.  Another part of the puzzle is the modulation of VGCC's.  Professor Tietz showed that chronic BZD exposure significantly reduces the action potential voltage necessary to activate the high voltage L-type VGCC's.  Those channels then allow a significant increase in intracellular calcium levels and subsequent neuronal excitability.  I think this is why gabapentin was a miracle for me in the beginning but isn't any longer due to tolerance to it. 

 

RST

 

Hi RST. Do you have any literature/links of the high voltage L-type VGCC's? I would love to read. Thank you.

[[Re...]]

Hi Liberty

 

I'm not saying exclusively by GCPR's.  It is but one process.  Another part of the puzzle is the modulation of VGCC's.  Professor Tietz showed that chronic BZD exposure significantly reduces the action potential voltage necessary to activate the high voltage L-type VGCC's.  Those channels then allow a significant increase in intracellular calcium levels and subsequent neuronal excitability.  I think this is why gabapentin was a miracle for me in the beginning but isn't any longer due to tolerance to it. 

 

RST

 

Hi RST. Do you have any literature/links of the high voltage L-type VGCC's? I would love to read. Thank you.

 

Hi, LorazepamFree.

 

Yes, I do have links.  If you bear with me for a few days, I'll dig them up.

 

-RST

[[li...]]

Possibly I'm going to be a bit against the intentions of the author regarding letting this thread slide off the first page of this section just once;

 

It's indeed not a thread for the faint hearted.

 

I don't believe everyone heals. If you have been on high doses of benzodiazepines for many years, are older, let's say you're mixing 4 mg clonazepam with 3 mg alprazolam, add high levels of chronic physical or mental physical stress not related to the drug, take drugs that disrupt other neurotransmitters in ways that mess up your brain, expose yourself to a course of prednisone and then stop C/T, become a dysfunctional human wreck the odds are that you will not heal (fully) !

 

'You will heal no matter what ' No. It matters what happens. Maybe not if you've only been on 10 mg diazepam for 6 months, but there are limits to what the body can endure.

I think that's an important point. I only wish my 'first' GP had gotten that.

[[co...]]

Thank you for this thread.

 

Must revisit when my cognition is online.

[[Be...]]

Dr. Ashton said that people should have good support.  Boy, I sure don't have that.  I live alone and have had nothing but unrelenting stress on me ever since I got off these retched pills.  I'm getting worse because all this external stress on me is killing off my brain cells and causing serious glutamate storming each and every day.  I never get a break from all the stress on me and it makes me so very sick. 

[[Lo...]]

Dr. Ashton said that people should have good support.  Boy, I sure don't have that.  I live alone and have had nothing but unrelenting stress on me ever since I got off these retched pills.  I'm getting worse because all this external stress on me is killing off my brain cells and causing serious glutamate storming each and every day.  I never get a break from all the stress on me and it makes me so very sick.

 

Yes. Sorry about the suffering, Becks. I wish I had better support myself. I don't think I would have ended up on these strong tranquilizers if I'd had more support. Wish I knew where to find it. We live in such a dog-eat-dog world. I keep getting these neurological storms several times a day and wonder if I'll ever get off of these prescriptions and wonder if I really should. I know it sounds very un-recovery, but my own life and my mother's are at stake here.

 

 

[[Lo...]]

 

Healing Trauma Recovery - Guided Meditation for Relaxation, PTSD, Anxiety and Sleep

[[Re...]]

Hi Liberty

 

I'm not saying exclusively by GCPR's.  It is but one process.  Another part of the puzzle is the modulation of VGCC's.  Professor Tietz showed that chronic BZD exposure significantly reduces the action potential voltage necessary to activate the high voltage L-type VGCC's.  Those channels then allow a significant increase in intracellular calcium levels and subsequent neuronal excitability.  I think this is why gabapentin was a miracle for me in the beginning but isn't any longer due to tolerance to it. 

 

RST

 

Hi RST. Do you have any literature/links of the high voltage L-type VGCC's? I would love to read. Thank you.

 

Hi, LorazepamFree.

 

Yes, I do have links.  If you bear with me for a few days, I'll dig them up.

 

-RST

 

HELLO!!!!

 

SORRY IT TOOK ME SO LONG!!!  Here is a link to the aforementioned.  Now, it looks at the affect of diazepam and it makes the remark that it might not happen at therapeutic doses but I think other benzos like lorazepam or clonazepam may have more of an effect.  I read in another paper that I have to find that Clonazepam DOES also act on VGCC's.

 

http://jpet.aspetjournals.org/content/327/3/872.long?utm_source=TrendMD&utm_medium=cpc&utm_campaign=J_Pharmacol_Exp_Ther_TrendMD_0

 

All the best,

 

-RST

[[li...]]

Dr. Ashton said that people should have good support.  Boy, I sure don't have that.  I live alone and have had nothing but unrelenting stress on me ever since I got off these retched pills.  I'm getting worse because all this external stress on me is killing off my brain cells and causing serious glutamate storming each and every day.  I never get a break from all the stress on me and it makes me so very sick.

 

That's a good one. While on a personal level my support wasn't great but not a problem, I did have a GP who was intent on undermining my health and tapering or possibly early C/T !

That pretty much beats everything.

[[Lo...]]

Bump.