Retigabine (Trobalt, Potiga) — General Discussion

If anyone uses trobalt or is considering using it...I'd recommend you take this-

Antioxidants are your body's primary way to neutralize free radicals -- those harmful metabolic byproducts that damage cells and tissues throughout your body.

Scientific evidence has repeatedly demonstrated that antioxidants are a cornerstone in the promotion of heart health, boosting your immune system, and memory support. They also appear to play a role in helping to slow your signs of aging.

Although many foods contain antioxidants, today's poor-quality diets are nearly always insufficient in the full range of these beneficial free radical scavengers.

So when you consider that the antioxidant potency of krill oil is 48 times more potent than fish oil, well… choosing between the two is easy.

If you're still not convinced of the antioxidant powers to krill oil, independent ORAC evaluations have also established that genuine krill oil contains:

  • Over 300 times the antioxidant power of vitamin A and vitamin E
  • Over 47 times the antioxidant power of lutein
  • Over 34 times the antioxidant power of coenzyme Q-10
Pretty impressive, wouldn't you say?

To top it all off, krill oil also contains astaxanthin – a unique marine-source flavonoid – that creates a special bond with the EPA and DHA, which allows direct metabolism of the antioxidants, making them more bioavailable.
 
To top it all off, krill oil also contains astaxanthin – a unique marine-source flavonoid – that creates a special bond with the EPA and DHA, which allows direct metabolism of the antioxidants, making them more bioavailable.
What a great copy and paste danny! Trouble is there are always two sides of every argument and it is argued that taking supplements to a naturally healthy diet is very bad indeed and in fact some supplements have been shown to be bad for a person as they are for example too concentrated - just an example.....and just a thought...
 
If anyone uses trobalt or is considering using it...I'd recommend you take this-

Antioxidants are your body's primary way to neutralize free radicals -- those harmful metabolic byproducts that damage cells and tissues throughout your body.

Scientific evidence has repeatedly demonstrated that antioxidants are a cornerstone in the promotion of heart health, boosting your immune system, and memory support. They also appear to play a role in helping to slow your signs of aging.

Although many foods contain antioxidants, today's poor-quality diets are nearly always insufficient in the full range of these beneficial free radical scavengers.

So when you consider that the antioxidant potency of krill oil is 48 times more potent than fish oil, well… choosing between the two is easy.

If you're still not convinced of the antioxidant powers to krill oil, independent ORAC evaluations have also established that genuine krill oil contains:

  • Over 300 times the antioxidant power of vitamin A and vitamin E
  • Over 47 times the antioxidant power of lutein
  • Over 34 times the antioxidant power of coenzyme Q-10
Pretty impressive, wouldn't you say?

To top it all off, krill oil also contains astaxanthin – a unique marine-source flavonoid – that creates a special bond with the EPA and DHA, which allows direct metabolism of the antioxidants, making them more bioavailable.
anti oxidants actually don`t protect you more against free radicals ... because you take the anti oxidant the cells will naturally not build a protection against these free radicals ... however when you don`t take them the cells will protect and this will lead to less damage ...

http://www.ucl.ac.uk/~ucbtdag/Wenner_2013.pdf
 
i`m starting to think it is actually the GABA in RTG that is silencing the T ... cuase GABA is the neurotransmitter the inhibits neural overstimulation by glutamate ... so it connects to the synaps so it blocks other neurotransmitters from being able to stimulate or influence the transmitter ... and that is why we feel so incompetent on RTG ... alot of pathways or inhibited by GABA ... any thoughs on it someone?

side note, this is my simple understanding after reading this and this

http://www.vitalityandwellness.com.au/health-blog/low-gaba-levels-increase-gaba-naturally

http://www.naturalhealthadvisory.co...eficiency-symptoms-you-can-identify-yourself/
 
i`m starting to think it is actually the GABA in RTG that is silencing the T ... cuase GABA is the neurotransmitter the inhibits neural overstimulation by glutamate ... so it connects to the synaps so it blocks other neurotransmitters from being able to stimulate or influence the transmitter ... and that is why we feel so incompetent on RTG ... alot of pathways or inhibited by GABA ... any thoughs on it someone?

side note, this is my simple understanding after reading this and this

http://www.vitalityandwellness.com.au/health-blog/low-gaba-levels-increase-gaba-naturally

http://www.naturalhealthadvisory.co...eficiency-symptoms-you-can-identify-yourself/

"GABA receptor antagonists are drugs which inhibit the action of GABA. In general these drugs produce stimulant and convulsant effects, and are mainly used for counteracting overdoses ofsedative drugs.

Examples include bicuculline and metrazol, and the benzodiazepine GABAA receptor antagonist flumazenil.

Also thujone and muira puama[citation needed] may have properties of GABAA receptor antagonism."
 
"GABA receptor antagonists are drugs which inhibit the action of GABA. In general these drugs produce stimulant and convulsant effects, and are mainly used for counteracting overdoses ofsedative drugs.

Examples include bicuculline and metrazol, and the benzodiazepine GABAA receptor antagonist flumazenil.

Also thujone and muira puama[citation needed] may have properties of GABAA receptor antagonism."
That doesn`t mean anything ... I`m not speaking about antagonists ... but GABA protagonists ... GABA stimulation ... what you copied is drugs that inhibit GABA action ...Epilepsy is a convulsion so drugs that stimulata convulsion is not what we look for.

What is GABA?

Neurotransmitters are the chemical messengers used by neurons to communicate with one another and with other types of cells. Every neurotransmitter behaves differently; inhibitory neurotransmitters tend to calm, while excitatory neurotransmitters tend stimulate the brain. GABA's primary function as the brain's major inhibitory neurotransmitter is to prevent overstimulation. It does this by counteracting glutamate—the brain's major excitatory neurotransmitter. When GABA binds to a receptor, it prevents stimulation by glutamate. When GABA levels are inadequate, overstimulation due to high levels of glutamate can occur and lead to symptoms of low GABA.
 
That doesn`t mean anything ... I`m not speaking about antagonists ... but GABA protagonists ... GABA stimulation ... what you copied is drugs that inhibit GABA action ...Epilepsy is a convulsion so drugs that stimulata convulsion is not what we look for.

What is GABA?

Neurotransmitters are the chemical messengers used by neurons to communicate with one another and with other types of cells. Every neurotransmitter behaves differently; inhibitory neurotransmitters tend to calm, while excitatory neurotransmitters tend stimulate the brain. GABA's primary function as the brain's major inhibitory neurotransmitter is to prevent overstimulation. It does this by counteracting glutamate—the brain's major excitatory neurotransmitter. When GABA binds to a receptor, it prevents stimulation by glutamate. When GABA levels are inadequate, overstimulation due to high levels of glutamate can occur and lead to symptoms of low GABA.



"Retigabine acts as activator of voltage – gated potassium channels ("M-channels"). It induces neuronal hyperpolarization and stabilization of the membrane resting potential (3). Another mechanism of action involves GABA. Kapetanovic MP et al. (1995) (4) showed increased synthesis of GABA in rat hipocampal slices. The enhanced chloride current, induced by GABA is not caused by activation of benzodiazepine receptors (5). Sills GJ et al. (2000) (6) reported that Retigabine diminish the concentrations of glutamate and glutamine in mouse brain."
 
"Retigabine acts as activator of voltage – gated potassium channels ("M-channels"). It induces neuronal hyperpolarization and stabilization of the membrane resting potential (3). Another mechanism of action involves GABA. Kapetanovic MP et al. (1995) (4) showed increased synthesis of GABA in rat hipocampal slices. The enhanced chloride current, induced by GABA is not caused by activation of benzodiazepine receptors (5). Sills GJ et al. (2000) (6) reported that Retigabine diminish the concentrations of glutamate and glutamine in mouse brain."
I`m happy to read that it is `not caused by activation of benzodiazepine receptors` ... complete diffrent action ... Good, makes it clearer ... every bit more understanding :)
 
i`m starting to think it is actually the GABA in RTG that is silencing the T


Interestingly enough this company is looking into something to do with GABA and NDMA and says the below on their research program page


Discovery Programs
We are exploring additional potential products in a variety of CNS disorders based on modulation of both the GABAA and NMDA receptors. In addition to our products focused on status epilepticus (SE), other central nervous system (CNS) disorders we believe our approach may have a significant impact on include Rett syndrome, Dravet syndrome, fragile X syndrome, anxiety, depression, sleep disorders, mania, tremor, tinnitus and post-traumatic stress disorder.


Link to the program page the above came from

http://www.sagerx.com/programs.php
 
@nills, do benzos have the same effect on your T as RTG? If it's truly just a GABA thing then I'd suspect that a couple milligrams of clonazepam would do the same thing.

I'm trying hard to make it to the 5 year mark without benzos before I get on that bus again, but if I get another 36 months under my belt and things haven't improved I may just say fuck it and take kpin again. It's not great and I'd vastly prefer to not be on it forever, but taking RTG forever isn't even slightly an option.
 
Thats good you can get it prescribed, think Canada Dr will prescibe it? I need to check out with him or a Neurologist I wonder if I can get it covered by my disability
 
@nills, do benzos have the same effect on your T as RTG? If it's truly just a GABA thing then I'd suspect that a couple milligrams of clonazepam would do the same thing.

I'm trying hard to make it to the 5 year mark without benzos before I get on that bus again, but if I get another 36 months under my belt and things haven't improved I may just say fuck it and take kpin again. It's not great and I'd vastly prefer to not be on it forever, but taking RTG forever isn't even slightly an option.
Hi linearb,
I have never taken a benzo, except once as a party drug (rohypnol) .. I also prefer not to go that route. I only want to invest my health to see if it influences my T. I just had a week - 10 days of very loud T. I was on a high dose of cortisoids for this time for my TMJ (Celestone). The drug made it worse while on it ... but since I stopped few days ago my T has been fairly low the last 2 days. i hope it will stay like this (of course) ... I will continue with Trobalt and maybe even try Neurontin or Sulpiride. I`m only afraid it will create permanent changes in the wrong direction as I have read this can happen with GABA. somewhere ... But my neurologist told me that all the cognitive changes of Trobalt or Keppra only last the time you are on it and fade the longer you take it. They do not create permanent damage to your intelligence or something like that. That was a relief to hear.

Do you mean you took 50mg of Trobalt? ... the first 50 mg Trobalt definately had an effect on my T and feeling a bit doped for an hour ... 100 did it also, than 200 did little to nothing and 300 a bit .. .but than 400 again was major influence ... it comes in waves the ffect of Trobalt. But the high doses were the best. They create a steady decline of the noise ... instead of the peaks that lower doses create ... on Trobalt I was waking up in near silence .. even after a 10-12 hour gap between the last dose ... oooh the sweet peace and joy those monrings were ... or just sitting in the city drinking a coffe looking at the trees and sky in silence ... realising this is what 85 percent of the world experienes everyday ... and still they run around like frightend ghosts ... if only they knew they are bathing in the deepest inner silence ... they would shut up and keep quiet ;)
 
@nills, do benzos have the same effect on your T as RTG? If it's truly just a GABA thing then I'd suspect that a couple milligrams of clonazepam would do the same thing.

I'm trying hard to make it to the 5 year mark without benzos before I get on that bus again, but if I get another 36 months under my belt and things haven't improved I may just say fuck it and take kpin again. It's not great and I'd vastly prefer to not be on it forever, but taking RTG forever isn't even slightly an option.

"Retigabine acts as activator of voltage – gated potassium channels ("M-channels"). It induces neuronal hyperpolarization and stabilization of the membrane resting potential (3). Another mechanism of action involves GABA. Kapetanovic MP et al. (1995) (4) showed increased synthesis of GABA in rat hipocampal slices. The enhanced chloride current, induced by GABA is not caused by activation of benzodiazepine receptors (5). Sills GJ et al. (2000) (6) reported that Retigabine diminish the concentrations of glutamate and glutamine in mouse brain."
 
I got the slight dopey/drowsy feeling, but really no impact on my T :-/ I'll stick with 3x50 for a few days, though...

Just go up and see what happens ... RTG is not the Devil we sometimes make it out to be ... for myself I belief from all the info I have rad so far that all the major negative side effects happen after long term use ... as long as you stay under 4-5-6 months ... it`s all good IMO..

try to listen to your T when the dopey feeling starts .. .you will start to see the sound will morph into diffrent sounds and sometimes goes away completely ... it lasts only little while on 50 mg`s ... maybe 10 minutes ... but something happens ... for sure
 
Just tried once 300mg dose - I only have enough pills to do it again today before sleep and my overall thoughts are that anyone counting on RTG to quiet his T 100% need to get his hopes scaled down.
took 50mgs. feel a little druggy. I realize that some people think you need to get up to fairly alarming doses before it does anything, but if I don't see any impact whatsoever in my T at lower doses, I may not really be willing to just escalate up and up for weeks.
i had first real effect at 300mg. I didnt taper up. Tried 9 times 100mg, 3 times 200mg and 2 times 300mg. At 300mg i was drugged for 2 hours ater 1 to 2 hours. I didnt taper up. Had slight chest pain. Minor urination retention. Lot of anxiety.

I think taper up is to make sure to your heart and kidneys can take it. Possibly to know minimal dose for epilepsy too.

As for for my T i didnt have much of a dofference but something was hapenning. Today after 2x300mg my t is kinda clearer and less crickets more like waterfall. I hope you get better and more conclusive results than me. Good luck and dont be too concerned with side effects, try yo taper up as soon as you feel safe on dosage you are.
 
After my brief experiences with 2x50mg yesterday, I think I am going to shelve this idea until I've explored rTMS and possibly a couple other things, for four reasons:
* the effects of 50mg were such that I was cognitively impaired to a point where it made it difficult to do my job, so I believe that escalating to a significant dose would possibly make me unable to perform my usual duties.
* despite being strongly intoxicating, this had no impact on my tinnitus whatsoever. So, it's not 'hitting a button' like I hoped it might (and like some people have reported).
* even if escalating to a higher dose did 'hit a button', I'd have difficulty working, and also be in a situation where I am taking a relatively dangerous drug for symptomatic relief... I do not believe that I can stay on it for a long period of time with any certainty that it's not going to lead to worse problems, so, what's the point? Taking a six month vacation from my T at the expense of kidney damage / potential vision loss sounds like a bad tradeoff.
* there are several other therapies I want to explore before playing chemical roulette, probably starting with the rTMS protocol from the VA study.

I think this is an extremely dangerous drug. I believe that I might be more comfortable taking benzos for an extended period again than taking this drug for a short period of time. Benzos have a lot of problems associated with their long term use, but, they have been in the world for a half century, hundreds of millions of people have indeed used them long term, and that actual severe side effects appear to be limited to a much smaller subset of users than RTG's severe side effects. RTG is much less thoroughly studied, but don't think the severe effects only appear after really protracted use: skin/eye discoloration has been documented with as little as 4 months of use, and among people who did take the drug for a number of years, 30% showed visual anomalies. That's vastly higher than the really scary edge cases among benzo users.

I think RTG is safer than suicide, but I'd be very hard pressed to call it safer than benzos, even for relatively short-term use.
 
After my brief experiences with 2x50mg yesterday, I think I am going to shelve this idea until I've explored rTMS and possibly a couple other things, for four reasons:
* the effects of 50mg were such that I was cognitively impaired to a point where it made it difficult to do my job, so I believe that escalating to a significant dose would possibly make me unable to perform my usual duties.
* despite being strongly intoxicating, this had no impact on my tinnitus whatsoever. So, it's not 'hitting a button' like I hoped it might (and like some people have reported).
* even if escalating to a higher dose did 'hit a button', I'd have difficulty working, and also be in a situation where I am taking a relatively dangerous drug for symptomatic relief... I do not believe that I can stay on it for a long period of time with any certainty that it's not going to lead to worse problems, so, what's the point? Taking a six month vacation from my T at the expense of kidney damage / potential vision loss sounds like a bad tradeoff.
* there are several other therapies I want to explore before playing chemical roulette, probably starting with the rTMS protocol from the VA study.
Potassium channel modulator drugs require the patient getting used to them. Cognitive side-effects will wear off to some degree (with time).
 
Potassium channel modulator drugs require the patient getting used to them. Cognitive side-effects will wear off to some degree (with time).
I am aware of this and I stand by everything I said in my previous post. Believe me, before I even considered going down this route I consumed every available piece of information.

edit: I'm not trying to discourage anyone else from going this route, I am just explaining why I'm not doing so at this time.
 
I am aware of this and I stand by everything I said in my previous post. Believe me, before I even considered going down this route I consumed every available piece of information.

edit: I'm not trying to discourage anyone else from going this route, I am just explaining why I'm not doing so at this time.

Seriously. How does passerby know so much about potassium channel modulators, when he's only been on here since July? Very strange. Few weeks ago, he didn't know how to inbox people. This week he knows so much about how these drugs works, that he could write an essay on them. Am I the only one baffled? Has he taken trobalt before?

Anyway, Linerab. I would be very careful with trobalt, as it can cause serious problems with eyesight and kidneys. I have noticed some visual acuity has diminished and that it can cause issues with kidneys. I had so many water infections that it just was out of the ordinary, to the point where my kidneys had become infected and my white cell blood count was elevated to 16. I also have so many bloody floaters from taking it. The drug is dangerous and should be off the market and revised for safety. I was desperate, but I will never ever take trobalt again. If the devil created drugs, trobalt would be his masterpiece.
 
Anyway, Linerab. I would be very careful with trobalt, as it can cause serious problems with eyesight and kidneys. I have noticed some visual acuity has diminished and that it can causes issues with kidneys. I had so many water infections that it just was out of the ordinary, to the point where my kidneys had become infected and my white cell blood count was elevated to 16. I also have so many bloody floaters from taking it. The drug is dangerous and should be off the market and revised for safety. I was desperate, but I will never ever take trobalt again. If the devil created drugs, trobalt would be his masterpiece.

Yikes, that's good to know.

If I had T of much more recent onset, I might be a lot more willing to mess with this (or AM-101). I'm just not convinced they're going to do much for me at this stage of the game. If Autifony hits the market, that might be a different story -- and I am interested in pursuing rTMS. Based on the limited data that only works for ~50% of people, but both studies to date have shown that it can be effective in people with long-standing, drug-resistant T.
 

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