Study: GABA can Help Overcome Caffeine Sleep Issues

CFC

CFC

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Caffeine making you sleep badly? GABA helps

"Weight loss and energy supplements that contain caffeine generally work fine, but they can mess around with your sleep. Researchers at Konkuk University in South Korea think they may have discovered a solution to this problem. Their animal studies suggest that GABA supplementation can cancel out the negative effects that caffeine has on sleep......."


Read the rest here


And if you add some glycine and glutamine to the GABA before bed you'll get a nicely amplified GH spike as well as better sleep, particularly so if using GHRPs...
 
Caffeine never really affects my sleep. I guess I'm lucky. Though for me, any sleep issues: clonidine. My fix all lol.
 
Im one of the few who doesnt drink coffee or really anything with caffeine, ive never liked any type of stimulants even something as mild as caffeine
 
From what I understand is that GABA is an hyperpolarizing neurotransmitter that inhibits the action potential at whatever relevant neuronal synapse. Does the threshold potential for decreasing activity reach a limit in how much it can inhibit the stimuli from caffeine? I noticed the study was only mimicing a "strong cup of coffee", but we all know that majority of coffee drinkers far exceed that intake volume. So would the calming effect be subjective to the total amount of caffeine consumed?

The study compared the effects to utilizing a barbitutate, which is recognized to interact predominantly with the GABAA receptor. (GABA C receptors showed highest sensitivity) [1] Would the supplementation of GABA work across the whole spectrum of GABA receptors? I always had the theory that supplementing further upstream with precursor compounds emitted a greater activity once the metabolic processes reached downstream in the conversion. (notably with L-Tryptophan helping increase natural serotonin/melatonin secretion)

From my own little science projects I've noticed that if you try to increase dosages beyond the concentrations that would be found in normal physiological terms that it will increase your probability to wake up groggy from the inhibitory/sedative activities.

Since I've seen GABA referenced with increasing insulin sensitivity and GH secretion post exercise at the bottom of that study. So I'm assuming its inhibitory activities are presynaptic? We learned about this a little bit, but its something like binding to the chloride ion channel causing an influx and increasing the negativity at the cell membrane leading to less action potential... correct me if I'm wrong.

Does the inhibitory activities have an accumulative effect if administered throughout the day on a continuous basis? Can saturation occur or is the nervous system able to internally regulate it's own signaling? I've been noticing that a lot of cellular metabolic interactions have a positive modulation vs. negative with their allosteric regulation.


EDIT: I answered my own question about presynaptic vs. postsynaptic inhibition. GABA's increase to resting potential negativity (hyperpolarization) is considered a inhibitory postsynaptic potential (IPSP)[2]





[1] http://www.ncbi.nlm.nih.gov/pubmed/11983310
[2] https://www.dnalc.org/view/485-GABA-Neurotransmitter.html
 
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GrymReefer said:
Does the threshold potential for decreasing activity reach a limit in how much it can inhibit the stimuli from caffeine?
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Probably, in the same way that the excitatory effect of increasing caffeine diminishes. But also, don't forget GABA poorly crosses the BBB - there may be some kind of threshold/maximal (saturation) uptake on that vector that does not exist with caffeine.

GrymReefer said:
So would the calming effect be subjective to the total amount of caffeine consumed?
Click to expand...

I'm sure it would (combined with tolerance effects). There aren't many off/on switches in the body really.

GrymReefer said:
Would the supplementation of GABA work across the whole spectrum of GABA receptors?
Click to expand...

I think we could assume it does. However, the important factor is likely to be where the specific receptor is (what part of the brain/CNS), and what relative concentration of receptors exist in that location. Some substrate-receptor ligands/complexes may outlast others as well, producing a time-delayed effect on your A/B/C effect. There's likely to be interaction with other systems as well (eg glutamate, NMDA etc) which would alter outcomes.

GrymReefer said:
I always had the theory that supplementing further upstream with precursor compounds emitted a greater activity once the metabolic processes reached downstream in the conversion. (notably with L-Tryptophan helping increase natural serotonin/melatonin secretion)
Click to expand...

Not sure I understand you here. Are you saying that you have greater success with precursor substrates like Tryptophan than actually ingesting melatonin or 5-HTP?? If so that's an unusual experience.

GrymReefer said:
Does the inhibitory activities have an accumulative effect if administered throughout the day on a continuous basis? Can saturation occur or is the nervous system able to internally regulate it's own signaling? I've been noticing that a lot of cellular metabolic interactions have a positive modulation vs. negative with their allosteric regulation.
Click to expand...

Sort of covered that a bit above. But I would speculate that the inhibitory activity would diminish if used continuously, like with most compounds.
 
Not sure I understand you here. Are you saying that you have greater success with precursor substrates like Tryptophan than actually ingesting melatonin or 5-HTP?? If so that's an unusual experience.
Click to expand...

L-Tryptophan and 5-HTP eventually turn into N-Acetylserotonin (NAS). However, starting with L-Tryptophan provides the reduction to the reuptake of serotonin in comparison to starting with 5-HTP. I would only assume that the SSRI activity would be beneficial in allowing the body to properly produce the correct amount of serotonin and allow its sustained circulation from the interaction with SRU sites.

The exact volume of serotonin requested could differ if this step is skipped and instead opts to start at the cellular pathway of 5-HTP. NAS regulates the total conversion of serotonin>melatonin and increasing the potential for more favorable serotonin activity following the enzymatic alteration.

5-HTP production is also after the initial conversion of L-Tryptophan into tryptamine which greatly contributes to neurotransmitter regulation most notably controlling circadian rhythm.

Taking synthetic melatonin prior to bedtime caused morning groggyness that was potentiated from higher dosages, but I couldn't replicate the associated groggyness with L-Tryptophan. (even with supraphysiological dosages) I'm guessing it was most likely due to the leftover that wasn't utilized during sleep. Most melatonin I took at once was 10mg and it had the complete opposite effect on providing help with sleep. (Insomnia, restlessness, hunger, wake time disassociating/sedating feeling.)

Of course I can't validate anything I said and its all theoretical nonsense really. :)

L-Tryptophan: Basic Metabolic Functions, Behavioral Research and Therapeutic Indications
 
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GrymReefer said:
The study compared the effects to utilizing a barbitutate, which is recognized to interact predominantly with the GABAA receptor. (GABA C receptors showed highest sensitivity) [1] Would the supplementation of GABA work across the whole spectrum of GABA receptors? I always had the theory that supplementing further upstream with precursor compounds emitted a greater activity once the metabolic processes reached downstream in the conversion. (notably with L-Tryptophan helping increase natural serotonin/melatonin secretion)



Since I've seen GABA referenced with increasing insulin sensitivity and GH secretion post exercise at the bottom of that study. So I'm assuming its inhibitory activities are presynaptic? We learned about this a little bit, but its something like binding to the chloride ion channel causing an influx and increasing the negativity at the cell membrane leading to less action potential... correct me if I'm wrong.
Click to expand...

Although there is some research to suggest Magnesium binds to GABA sites and increases effect, also serotonin is another neurotransmitter that enhances GABA, and B-6 may increase GABA levels, while these supplements alter or potentiate the GABA receptor, they do not add any GABA to the system....
Oral GABA can affect the pancreas increasing insulin production, but GABA has been shown to increase prolactin...

There are conflicting study's but it is not thought GABA can pass the blood brain barrier in sufficient amounts to produce effect...





GABA works by binding GABA receptors on the postsynaptic neuron, opening chloride ion channels...
 
Edit: in ref to Grym's post:

I think you're just finding a roundabout way of saying that supplying adequate substrate will allow the brain to convert as much as required (but probably not more) for whatever function is needed :)

EG: 10mg of melatonin is such a supraphysiological amount that you have to expect it to cause unwanted side-effects. Conversely a shed-load of L-Tryp is unlikely to have anything like the same effect since (as its upstream, as you pointed out) it relies on conversion via pre-existing metabolic systems. The more of these pathways between a substrate and target, the more modulated you can expect the outcome to be.
 
Daz-69 said:
but GABA has been shown to increase prolactin...
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I should point out for anyone adding these supplements for GH effects that glycine also raises PRL. Most of these GH boosting substances are intrinsically tied into DA-PRL-GH system. Similar for GHRPs as well, even Ipamorelin which is (inaccurately, even in literature) claimed to not raise PRL.
 
CFC said:
Edit: in ref to Grym's post:

I think you're just finding a roundabout way of saying that supplying adequate substrate will allow the brain to convert as much as required (but probably not more) for whatever function is needed :)

EG: 10mg of melatonin is such a supraphysiological amount that you have to expect it to cause unwanted side-effects. Conversely a shed-load of L-Tryp is unlikely to have anything like the same effect since (as its upstream, as you pointed out) it relies on conversion via pre-existing metabolic systems. The more of these pathways between a substrate and target, the more modulated you can expect the outcome to be.
Click to expand...

Ironically I encounter people talking about taking those dosages consistently. They wonder why sleep is foreign to their brains!?

So would producing an inhibitory activity on the presynaptic neurons from GABA cause a more consistent wide spread reduction to the synapses excitability? Taking into consideration CFC mentioning he more pathways between substrate and target, the more modulated outcome.

but GABA has been shown to increase prolactin...
Click to expand...

Only thing that would concern me is if you were on cycle that also contained something that had interactions with prolactin secretion (trenabolone's agonist activity with prolactin levels and the increasing the likelihood of estrogenic activity)
 
I take 10mg melatonin every night. For probably two year now. Yet a great night of sex with the ol lady and I sleep like a baby without issue even on tren. Idk, sex with her just fully relaxes me and knocks my ass out. Her back massages leave me half asleep and drooling lol.

Edit: in regards to b6 potentiating melatonin I can't say yes or no as I've taken two different melatonin supps, same mg of melatonin except one has some added b6 while the other didn't. No noticeable difference to me.
 
Serotonin101 said:
I take 10mg melatonin every night. For probably two year now. Yet a great night of sex with the ol lady and I sleep like a baby without issue even on tren. Idk, sex with her just fully relaxes me and knocks my ass out. Her back massages leave me half asleep and drooling lol.

Edit: in regards to b6 potentiating melatonin I can't say yes or no as I've taken two different melatonin supps, same mg of melatonin except one has some added b6 while the other didn't. No noticeable difference to me.
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I don't think biotin supplementation would have any arguable impact with an individual who doesn't show signs of biotin-related deficiency.

LOL 10mg of melatonin!!?!?!??! Holy sharkshit batman.

I'm sure endocytosis-mediated receptor downregulation could occur from constantly saturating the receptor sites. In a natural instance N-Acetylserotonin is the dictating factor in how much serotonin can continue along the pathway involving conversion to melatonin.
 
Yep 10mg. Comes in single tablets that are sublingual. I like em. Good sleep and good dreams. No grogginess either but that took some time.
 
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