http://www.benzo.org.uk/amisc/ashdiag.pdf
According to RP, progesterone and pregnenolone both act on the GABA receptor as agonists, while estrogen acts on the GABA receptor as an antagonist. GABA has similar protective inhibitory effects as glycine, found in gelatin.
This paper stated that tolerance builds to benzodiazepines, and the authors think it involves GABA receptor desensitization and N-methyl-D-aspartate (NMDA) receptor sensitization, because withdrawal is particularly harsh and includes excitation. RP stated that NMDA is a receptor activated by excitatory amino acids and should be minimized.
That's unavoidable with drugs. However, patients showed reduced symptoms and less medical visits if they successfully quit the drugs. They had less anxiety if they quit the drugs and were eventually free of withdrawal symptoms. Side effects on concentration and memory also disappeared. It doesn't appear that these drugs have any cognitive benefits in the long-term, quite the opposite. Alcohol is another GABA agonist, but it has harmful health effects like toxicity, so obviously it's not beneficial. Barbiturates stimulate GABA too, but they have similar long-term effects to benzodiazepines and also lead to tolerance. Opiates are harmful in general, so the endorphin agonists are out.
Receptors are pretty complicated. Caffeine is an adenosine antagonist that can lead to the receptor's sensitization, and yet it's healthy in many ways. Tianeptine avoids a backlash of serotonin receptor sensitivity somehow, because it only causes withdrawal symptoms at very high doses, and I'm guessing it's the same way for other antagonists like LSD. RP sometimes recommends dopamine agonists like lisuride.
I once read a source that stated that there was less brain GABA receptors and more brain norepinephrine receptors in hyperthyroidism and hypothyroidism showed the opposite pattern (I may have mixed them up, but whatever, I couldn't find the source), because the conditions would alter the amounts of GABA and norepinephrine. So one could expect progesterone/pregnenolone/GABA/glycine/alanine to reduce the amount/sensitivity of GABA receptors and estrogen/aspartate/glutamate to increase the amount/sensitivity of GABA receptors. Or vice versa on NMDA agonists. It would theoretically be the same way with NMDA antagonists, no chronic benefits because of receptor adaption.
I was interested in benzodiazepines because I found out they can slow breathing. By slowing breathing, one can allow CO2 to build up, which has protective benefits like reducing serotonin, histamine, and DNA methylation. Now I wonder which substances reduce the rate of respiration without building tolerance.
Progesterone increases the amount of CO2 that is retained in tissues, but it increases the rate of respiration. Study subjects that took epsom salt baths (magnesium salts) urinated out excess magnesium, limiting blood levels. Sodium increases CO2 production and reduces adrenalin, which may reduce respiration rate, but the kidney also limits the amount that can be retained. I'm taking high-dose niacinamide and taurine, but my respiration isn't slower. Acetazolamide, a carbon anhydrase inhibitor, increases respiration by tricking the body into thinking there is too much CO2. It also excretes sodium and potassium, while normally higher CO2 retains electrolytes and provides stability in the CO2 level this way.
GHB (Gamma hydroxybutyrate) appears to have withrawal and tolerance build up. It contains butyric acid, a short-chain saturated fatty acid, which is why GHB could be expected to have chronic positive effects. But it doesn't due to tolerance.
http://www.ncbi.nlm.nih.gov/pubmed/12837642
The NMDA antagonists I looked at are tolerance-forming, and I doubt any others would avoid this.
GABA itself or glycine are possible candidates, but I don't know whether they would cause receptor tolerance. I plan on trying them soon anyway.
So what's a substance that can chronically reduce respiration rate without tolerance? I can't seem to find any. In fact, I'm not sure if it's possible to activate GABA receptors without tolerance building up, and I'm not sure if substances like progesterone or glycine lead to receptor desensitization or a reduced number of receptors. It could also be possible to reduce respiration rate with serotonin antagonists like shrooms, LSD, or mescaline.
A few of you might say it's best to focus on general health, but that's what CO2 is. I think CO2 is the most general chemical of health in all living beings. It deserves more focus. One can improve diet to a certain extent, but if the person still breathes a lot, then that is neglecting the most improvable and possibly the most important aspect of their health. Gut health, for example, is important, but it doesn't just include eating the right food. CO2 can increase a person's capacity to digest food by increasing oxygen in the cells of the gastrointestinal tract, and prevent incomplete digestion of sugars, for example, which can feed bacteria and increase endotoxin formation.
According to RP, progesterone and pregnenolone both act on the GABA receptor as agonists, while estrogen acts on the GABA receptor as an antagonist. GABA has similar protective inhibitory effects as glycine, found in gelatin.
This paper stated that tolerance builds to benzodiazepines, and the authors think it involves GABA receptor desensitization and N-methyl-D-aspartate (NMDA) receptor sensitization, because withdrawal is particularly harsh and includes excitation. RP stated that NMDA is a receptor activated by excitatory amino acids and should be minimized.
That's unavoidable with drugs. However, patients showed reduced symptoms and less medical visits if they successfully quit the drugs. They had less anxiety if they quit the drugs and were eventually free of withdrawal symptoms. Side effects on concentration and memory also disappeared. It doesn't appear that these drugs have any cognitive benefits in the long-term, quite the opposite. Alcohol is another GABA agonist, but it has harmful health effects like toxicity, so obviously it's not beneficial. Barbiturates stimulate GABA too, but they have similar long-term effects to benzodiazepines and also lead to tolerance. Opiates are harmful in general, so the endorphin agonists are out.
Receptors are pretty complicated. Caffeine is an adenosine antagonist that can lead to the receptor's sensitization, and yet it's healthy in many ways. Tianeptine avoids a backlash of serotonin receptor sensitivity somehow, because it only causes withdrawal symptoms at very high doses, and I'm guessing it's the same way for other antagonists like LSD. RP sometimes recommends dopamine agonists like lisuride.
I once read a source that stated that there was less brain GABA receptors and more brain norepinephrine receptors in hyperthyroidism and hypothyroidism showed the opposite pattern (I may have mixed them up, but whatever, I couldn't find the source), because the conditions would alter the amounts of GABA and norepinephrine. So one could expect progesterone/pregnenolone/GABA/glycine/alanine to reduce the amount/sensitivity of GABA receptors and estrogen/aspartate/glutamate to increase the amount/sensitivity of GABA receptors. Or vice versa on NMDA agonists. It would theoretically be the same way with NMDA antagonists, no chronic benefits because of receptor adaption.
I was interested in benzodiazepines because I found out they can slow breathing. By slowing breathing, one can allow CO2 to build up, which has protective benefits like reducing serotonin, histamine, and DNA methylation. Now I wonder which substances reduce the rate of respiration without building tolerance.
Progesterone increases the amount of CO2 that is retained in tissues, but it increases the rate of respiration. Study subjects that took epsom salt baths (magnesium salts) urinated out excess magnesium, limiting blood levels. Sodium increases CO2 production and reduces adrenalin, which may reduce respiration rate, but the kidney also limits the amount that can be retained. I'm taking high-dose niacinamide and taurine, but my respiration isn't slower. Acetazolamide, a carbon anhydrase inhibitor, increases respiration by tricking the body into thinking there is too much CO2. It also excretes sodium and potassium, while normally higher CO2 retains electrolytes and provides stability in the CO2 level this way.
GHB (Gamma hydroxybutyrate) appears to have withrawal and tolerance build up. It contains butyric acid, a short-chain saturated fatty acid, which is why GHB could be expected to have chronic positive effects. But it doesn't due to tolerance.
http://www.ncbi.nlm.nih.gov/pubmed/12837642
The NMDA antagonists I looked at are tolerance-forming, and I doubt any others would avoid this.
GABA itself or glycine are possible candidates, but I don't know whether they would cause receptor tolerance. I plan on trying them soon anyway.
So what's a substance that can chronically reduce respiration rate without tolerance? I can't seem to find any. In fact, I'm not sure if it's possible to activate GABA receptors without tolerance building up, and I'm not sure if substances like progesterone or glycine lead to receptor desensitization or a reduced number of receptors. It could also be possible to reduce respiration rate with serotonin antagonists like shrooms, LSD, or mescaline.
A few of you might say it's best to focus on general health, but that's what CO2 is. I think CO2 is the most general chemical of health in all living beings. It deserves more focus. One can improve diet to a certain extent, but if the person still breathes a lot, then that is neglecting the most improvable and possibly the most important aspect of their health. Gut health, for example, is important, but it doesn't just include eating the right food. CO2 can increase a person's capacity to digest food by increasing oxygen in the cells of the gastrointestinal tract, and prevent incomplete digestion of sugars, for example, which can feed bacteria and increase endotoxin formation.
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