4 votes
Posted 20 September 2016 - 08:45 AM
Try it with no 5htp. Stay away from serotonergics and cholinergics. Try one of the DRIs above, and something as simple as wheat can inhibit the conversion to NE. Watch out for symptoms of high dopamine tho
I've tried Bupropion (NRDI) without luck. I didn't like it. What other DRIs that are better than bupropion?
Posted 21 September 2016 - 04:58 AM
Confident & Optimistic? it isn't that simple!
Also, if you have low Dopamine you'd not have strong sexual drive.
Usually low Serotonin circulation causes: High Acetylcholine, Constipation, Strong sexual drive, High risk taking, Insomnia and Low motivation.
and high Acetylcholine symptoms are usually: Muscle weakness, Tiredness, Agitation associated with Dysphoria, Intelligent but Poor Common sense, Anhedonia or Blunt emotions, Itching and Low Heart-rate.
Low Serotonin (Low Inhibitory) and High Acetylcholine (High Inhibitory) might cause intolerance for Stimulants and Cholinergics (I am not 100% sure about this, personal assumption!)
anyway, I still suggesting 5-HTP at least for 4 weeks and see what happens.
Today afternoon, I took 100mg 5-HTP, 1 and a half hour after that I had goosebumps to almost every song I listened too. I usually do not have goosebumps easily like that. What does this mean?
Dont want to be the "I told you so" guy, and I am really not that kind of guy.
it means a lift from anhedonia.
if 5-htp works, it'd work after at least 4-weeks of taking it.
what you had experienced might be placebo-effects, don't be too excited! too much excitement would burn your motivation of taking it due to high raise in expectations!
Posted 21 September 2016 - 05:04 AM
Confident & Optimistic? it isn't that simple!
Also, if you have low Dopamine you'd not have strong sexual drive.
Usually low Serotonin circulation causes: High Acetylcholine, Constipation, Strong sexual drive, High risk taking, Insomnia and Low motivation.
and high Acetylcholine symptoms are usually: Muscle weakness, Tiredness, Agitation associated with Dysphoria, Intelligent but Poor Common sense, Anhedonia or Blunt emotions, Itching and Low Heart-rate.
Low Serotonin (Low Inhibitory) and High Acetylcholine (High Inhibitory) might cause intolerance for Stimulants and Cholinergics (I am not 100% sure about this, personal assumption!)
anyway, I still suggesting 5-HTP at least for 4 weeks and see what happens.
Today afternoon, I took 100mg 5-HTP, 1 and a half hour after that I had goosebumps to almost every song I listened too. I usually do not have goosebumps easily like that. What does this mean?
Sounds like it reversed a long standing anhedonia.
I don't think so. 3 hours after taking 100mg 5-HTP, my mood went down, I felt sad, I talked to my girlfriend and cried without clear reasons, I just felt sad.
12h07 pm: 150mg Bupropion
5h13 pm: 100mg 5-htp
7h: have goosebumps easily when listening to music
9h mood went down dramatically, felt sad for no reasons, cried easily. It was definitely because of the 5-htp.
Individuals with social phobia have too much serotonin -- not too little
first of all, as I said earlier, don't get too much excited, if you want to know 5-htp works or not, you have to keep taking it for ~a month.
second, I take that "sudden cryings" a better sign of reversed Anhedonia instead of those goosebumps. its really a good sign!
third, Do you also have social phobia? you didn't mention that before; am I wrong?
Posted 21 September 2016 - 05:15 PM
first of all, as I said earlier, don't get too much excited, if you want to know 5-htp works or not, you have to keep taking it for ~a month.
second, I take that "sudden cryings" a better sign of reversed Anhedonia instead of those goosebumps. its really a good sign!
third, Do you also have social phobia? you didn't mention that before; am I wrong?
Are you serious? 5-HTP gave me terrible experience/reaction, I will never touch it again. I do not have social phobia, I do not have any kinds of depression, I just react poorly to cholinergic stuff, which includes caffeine + theanine (google search for caffeine acetylcholine and theanine acetylcholine), now I know why I felt uncomfortable when on caffeine+theanine or caffeine, theanine alone.
I am experimenting 1.2g (divided into 2 doses) Acetylcysteine a day now.
Posted 21 September 2016 - 05:40 PM
Posted 21 September 2016 - 07:16 PM
As for dopamine reuptake, catuaba and flowering quince appear not to be cholinergic. Might be worth a shot. If those fail, I'm leaning toward the nicotinic agonist idea. But an RC, like GTS-21. That has its own thread, and is probably the most anticipated alpha-7 agonist in the pipelines.
Posted 22 September 2016 - 02:22 AM
Posted 22 September 2016 - 10:16 AM
With a name like Junkmaster, I will have to agree in his conclusion of high sex drive. The fact that you (OP) have a girlfriend and didn't mention this before is a really good thing. I even noticed less masturbation while in a relationship (as to save up myself to be in the mood for here - I can ballvulating), so you may be spot on in your conclusion. The reason for this, and maybe it is counterintuitive, not for lack of dopamine, for any clean DRI without the norepinephrine boost will increase sex drive. Norepinephrine on the other hand, stabilizes sex drive for better or for worse depending on your metric of success. For me, an NRI or even a NDRI just lets me control my thoughts better. The NDRI does let a lot more sexual impulsivity through than a straight NRI.
What I'm saying is that an NDRI/NDRA combo is really something that you have room for. Women with average BMI don't usually need sex more than 4x a month, maybe more with unprotected sex due to the half life of semen being a few days, which can be addictive for its antidepressant properties. If you didn't know that... doesn't it make sense how braindead you get after blowing a huge load? You donate a chunk of your life force every time.
Wow that got intense...
Anyway, I do think that since you have room for that combo in your lifestyle, go for it. If it is too intense, then something like Cat's Claw will knock out the tension from your system overnight in my experience.
May you tell me exactly what substances I should try please? NDRI/NDRA is too broad for me.
Keep in mind that I do not like Bupropion, do not react with Mucuna and react poorly to cholinergic stuff. However, I had good result with Planetary Herbals Cordyceps power CS-4, although Cordyceps sinensis promotes M1 muscarinic acetylcholine receptor. Maybe I react well to muscarinic receptor agonist rather than nicotinic receptor agonist, cause I react poorly to Nicotine too.
Planetary Herbals Cordyceps power CS-4 (3 tablets) increased my digit span score (from 16 to 18). It contains:Cordyceps sinensis Mycelia CS-4 (0.1% adenosine) (which promotes M1 muscarinic acetylcholine receptor), Astragalus Root, Codonopsis Root, Adenophora Root, Eucommia Bark, Eleuthero Root, Bai-Zhu Atractylodes Rhizome and Ginger Root.
As for dopamine reuptake, catuaba and flowering quince appear not to be cholinergic. Might be worth a shot. If those fail, I'm leaning toward the nicotinic agonist idea. But an RC, like GTS-21. That has its own thread, and is probably the most anticipated alpha-7 agonist in the pipelines.
Can you suggest me exactly which Catuaba type and brand is good? There are many kinds of Catuaba on amazon with doubtful quality.
Moreover, I react badly to Nicotine, why did you think nicotinic agonist is a good idea for me?
Posted 22 September 2016 - 11:57 AM
Usually somebody gets blue from choline, nicotine lifts them up. Already established that muscarine inhibits dopamine, and it has a somewhat unpleasant effect in everyone. Just making logical assumptions here. I would give tobacco a few more chances (without getting hooked), I know my first nicotine experiences were fraught with anxiety and nausea... not at all indicative of a typical experience.
And I don't know man, I spent 6 minutes searching and found all these. Surely one is authentic?
Posted 23 September 2016 - 07:41 AM
Usually somebody gets blue from choline, nicotine lifts them up. Already established that muscarine inhibits dopamine, and it has a somewhat unpleasant effect in everyone. Just making logical assumptions here. I would give tobacco a few more chances (without getting hooked), I know my first nicotine experiences were fraught with anxiety and nausea... not at all indicative of a typical experience.
And I don't know man, I spent 6 minutes searching and found all these. Surely one is authentic?
- https://www.mountain...ba-bark/profile
- http://herbs-america...atuaba-extract/
- http://www.vitacost....catuaba-extract
- http://www.iherb.com...CFYMvgQodzT0JMg
- https://www.alibaba.....0.0.zo1yDf&s=p
Wrong. This study (Nucleus Accumbens Acetylcholine Receptors Modulate Dopamine and Motivation.) states that reducing muscarinic acetylcholine receptor will reduce invigoration of reward seeking, while reducing nicotinic receptors will improve invigoration of reward seeking. So to increase motivation, we should increase muscarinic acetylcholine receptors, NOT nicotinic receptor.
Environmental reward-predictive cues can motivate reward-seeking behaviors. Although this influence is normally adaptive, it can become maladaptive in disordered states, such as addiction. Dopamine release in the nucleus accumbens core (NAc) is known to mediate the motivational impact of reward-predictive cues, but little is known about how other neuromodulatory systems contribute to cue-motivated behavior. Here, we examined the role of the NAc cholinergic receptor system in cue-motivated behavior using a Pavlovian-to-instrumental transfer task designed to assess the motivating influence of a reward-predictive cue over an independently-trained instrumental action. Disruption of NAc muscarinic acetylcholine receptor activity attenuated, whereas blockade of nicotinic receptors augmented cue-induced invigoration of reward seeking. We next examined a potential dopaminergic mechanism for this behavioral effect by combining fast-scan cyclic voltammetry with local pharmacological acetylcholine receptor manipulation. The data show evidence of opposing modulation of cue-evoked dopamine release, with muscarinic and nicotinic receptor antagonists causing suppression and augmentation, respectively, consistent with the behavioral effects of these manipulations. In addition to demonstrating cholinergic modulation of naturally-evoked and behaviorally-relevant dopamine signaling, these data suggest that NAc cholinergic receptors may gate the expression of cue-motivated behavior through modulation of phasic dopamine
Btw, NAcysteine gave me slightly brainfog. Now my protocol is HIIT training + optizinc every other day and piracetam + 5 tablets Planetary Cordyceps Power CS-4+ 150 Magnesium + 6mg Boron everyday. This boost my confidence, well being and maybe testosterone.
Posted 23 September 2016 - 10:55 AM
Posted 23 September 2016 - 11:04 AM
Yeah but if you saturate yourself in nicotine, your body doesn't realize it has less receptors (until you stop).. because the nicotine puts the adjusted equilibrium above the old floor. same with a muscsrinic antagonist, it's only gonna start working when you stop taking it.
I'm sure the acetylecholine is an indirect concern. Best just to give the catuaba or flowering quince a try, and not overcomplicate things
Nicotine decreased my digit span scores.
I'm going to purchase this Catuaba: http://www.iherb.com...-oz-30-ml/13976, yet I cannot find a flowering quince supplement, which would you suggest?
Btw, I've bought some DXM but have not tried it cause 100mg 5-HTP made me depressed and I read somewhere DXM is serotonergic, hence I'm skeptical to try. What do you guys think?
Posted 25 September 2016 - 03:13 PM
Posted 26 September 2016 - 05:19 AM
NDRI/NDRA is broad on purpose. I was giving you a range of medications and supplements to try. The most effective ones for motivation are Mixed amphetamine salts (already know that is not available) and methylphenidate. There is also ephedrine and pseudoephedrine, which are highly regulated here in the USA, but still available in OTC doses for allergies and sickness. So I guess start there with one of those 3 remaining.
Ephedrine is cholinergic (the capacity of ephedrine to stimulate acetylcholine liberation) and I cannot buy Ritalin (methylphenidate) here. What else do you suggest for me?
Posted 26 September 2016 - 05:25 AM
Ok. Lots of good advice, I think, but it seems like we are all over the place. Back to the original post-- "I have very low motivation, I usually skip school, do not have ambition. I am a procrastinator.
I am confident, I do not have depression.
Exercise does not help, I exercise everyday."
We just need more info! How many confident people, not depressed, who exercise every day, do you know with low motivation? I can't think of one.
What are you doing when you skip school?
Why would you skip school if you are confident and have a normal sex drive? Isn't that where all the girl's your age are?
BTW Junk doesn't come from THAT Junk, it's because I run a lot of "junk" or slow miles as part of my exercise/meditation routine. By the time I realized I should have changed it, I thought, "Why bother...my posts should speak for themselves." I don't think I'm the most aggressive/macho type by a long shot. At least I sure hope I don't come across that way. I'm just a nootropic/ergo/body hacking fan nearing 50 and hate the idea my days of optimum performance are behind me. Too much still to do!
Posted 26 September 2016 - 05:46 AM
Ok. Lots of good advice, I think, but it seems like we are all over the place. Back to the original post-- "I have very low motivation, I usually skip school, do not have ambition. I am a procrastinator.
I am confident, I do not have depression.
Exercise does not help, I exercise everyday."
We just need more info! How many confident people, not depressed, who exercise every day, do you know with low motivation? I can't think of one.
What are you doing when you skip school?
Why would you skip school if you are confident and have a normal sex drive? Isn't that where all the girl's your age are?
BTW Junk doesn't come from THAT Junk, it's because I run a lot of "junk" or slow miles as part of my exercise/meditation routine. By the time I realized I should have changed it, I thought, "Why bother...my posts should speak for themselves." I don't think I'm the most aggressive/macho type by a long shot. At least I sure hope I don't come across that way. I'm just a nootropic/ergo/body hacking fan nearing 50 and hate the idea my days of optimum performance are behind me. Too much still to do!
When I skipped school in high school, I stayed at home and used my computer to learnt, researched about iOS scene, nowaday, I skipped school to stay at home playing computer game, researching nootropic to increase my motivation, surfing the web. A life like this is enough for me (although, of course I want to be something like the richest man in the world, but just likes this is ok too): eat, use computer, sleep. I think living a life like this is a waste of my ability. I am able to achieve more, but I cannot get myself to do. In my mind, it is ok to live like this, so how can I get myself to do?
I have a girlfriend so I do not try hard to meet up girls nowaday.
All in all, in my mind, I have two thoughts simultaneously: live like this (eat, use computer, sleep) and live not like this (do more interesting things). "Live like this" is 80% and "live not like this" is 20%, I want to reverse the proportion: "Live like this" 20% and "live not like this" 80%. I believe I have the ability to achieve "live not like this" lifestyle but cannot make up my mind
Edited by tronatula2, 26 September 2016 - 05:51 AM.
Posted 26 September 2016 - 10:48 AM
That's a study on peripheral nerves endings. Also, any increase in dopamine and norepinephrine is going to change acetylcholine activity. Neuromodulators tend to do that. Usually they increase activity. I know phenethylamine induces acetylcholine release, so then it would stand to reason that there is literally no sympathetic amine that would not have this activity and therefore a typical NDRA would have cholinergic effects, since most are analogues of phenethylamine.Ephedrine is cholinergic (the capacity of ephedrine to stimulate acetylcholine liberation) and I cannot buy Ritalin (methylphenidate) here. What else do you suggest for me?NDRI/NDRA is broad on purpose. I was giving you a range of medications and supplements to try. The most effective ones for motivation are Mixed amphetamine salts (already know that is not available) and methylphenidate. There is also ephedrine and pseudoephedrine, which are highly regulated here in the USA, but still available in OTC doses for allergies and sickness. So I guess start there with one of those 3 remaining.
Edited by devinthayer, 26 September 2016 - 11:46 AM.
Posted 26 September 2016 - 01:25 PM
Interesting bit from that examine link, devon. For comparison, Atomoxetine's Ki for DAT is 1451 and 5 for NET. Quinoa should be noticeably effective.
An extract of fructus akebiae containing 90% hederagenin by weight shows affinity for the dopamine transporter at a Ki of 1.03+/-0.04nM (stronger than the reference nomifensine) and prevented dopamine uptake.[8]
Hederagenin can be found in Chenopodium quinoa (the food product known as Quinoa[2][3]) in the flower, fruit, seed (edible portion[4] at 27-28% total saponins or 307.8-465mg per 100g dry weight, inclusive of all glycosides[5]), and seed coat.[6]
Got this 2005 study with some amazing graphs giving you an idea for just how active Catuaba is at the dopamine transporter! Not as good as atomexetine, but still quite powerful. You can see the rat responds well to 200mg/kg, about 2.2g for a human.
It doesn't look like the serotonin uptake tops out til around 1mg/mL (after the 0.3mL/mg reading, graph B). That's 65g for an adult. The in vitro dopamine release is doubled by the 10μg/mL dose (650mg for an adult) and tripled by the 20μg/mL dose (1300mg). For comparison... a 0.3mg/kg rat dose produces a 50% increase in dopamine while a 1mg/kg rat dose produces a near tripling of dopamine. In humans, this would be 12mg.
Flowering Quince is admittedly weaker (probably). The researchers are extremely vague in their findings... between 1 and 1000μg/mL increased dopamine by an undisclosed amount. That's between 65mg and 65g for a 65kg man. You would probably need 6.5g, but as Devin points out, even this dose is unlikely to hold a candle to 10mg atomexetine.
Dopamine transporter inhibitory and antiparkinsonian effect of common flowering quince extract.
Zhao G1, Jiang ZH, Zheng XW, Zang SY, Guo LH. (2008)
Common flowering quince (FQ) is the fruit of Chaenomeles speciosa (Sweet) Nakai. FQ-containing cocktails have been applied to the treatment of neuralgia, migraine, and depression in traditional Chinese medicine. The present study assessed whether FQ is effective in dopamine transporter (DAT) regulation and antiparkinsonism by utilizing in vitro and in vivo assays, respectively. FQ at concentrations of 1-1000 microg/ml concentration-dependently inhibited dopamine uptake by Chinese hamster ovary (CHO) cells stably expressing DAT (D8 cells) and by synaptosomes. FQ had a slight inhibitory action on norepinephrine uptake by CHO cells expressing the norepinephrine transporter and no inhibitory effect on gamma-aminobutyric acid (GABA) uptake by CHO cells expressing GABA transporter-1 or serotonin uptake by the serotonin transporter. A viability assay showed that FQ mitigated 1-methyl-4-phenylpyridinium-induced toxicity in D8 cells. Furthermore, in behavioral studies, FQ alleviated rotational behavior in 6-hydroxydopamine-treated rats and improved deficits in endurance performance in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Furthermore, immunohistochemistry revealed that FQ markedly reduced the loss of tyrosine hydroxylase-positive neurons in the substantia nigra in MPTP-treated mice. In summary, FQ is a selective, potent DAT inhibitor and has antiparkinsonian-like effects that are mediated possibly by DAT suppression. FQ has the potential to be further developed for Parkinson's disease treatment.
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Posted 26 September 2016 - 02:42 PM
Interesting bit from that examine link, devon. For comparison, Atomoxetine's Ki for DAT is 1451 and 5 for NET. Quinoa should be noticeably effective.
An extract of fructus akebiae containing 90% hederagenin by weight shows affinity for the dopamine transporter at a Ki of 1.03+/-0.04nM (stronger than the reference nomifensine) and prevented dopamine uptake.[8]
Hederagenin can be found in Chenopodium quinoa (the food product known as Quinoa[2][3]) in the flower, fruit, seed (edible portion[4] at 27-28% total saponins or 307.8-465mg per 100g dry weight, inclusive of all glycosides[5]), and seed coat.[6]
Got this 2005 study with some amazing graphs giving you an idea for just how active Catuaba is at the dopamine transporter! Not as good as atomexetine, but still quite powerful. You can see the rat responds well to 200mg/kg, about 2.2g for a human.
It doesn't look like the serotonin uptake tops out til around 1mg/mL (after the 0.3mL/mg reading, graph B). That's 65g for an adult. The in vitro dopamine release is doubled by the 10μg/mL dose (650mg for an adult) and tripled by the 20μg/mL dose (1300mg). For comparison... a 0.3mg/kg rat dose produces a 50% increase in dopamine while a 1mg/kg rat dose produces a near tripling of dopamine. In humans, this would be 12mg.
Flowering Quince is admittedly weaker (probably). The researchers are extremely vague in their findings... between 1 and 1000μg/mL increased dopamine by an undisclosed amount. That's between 65mg and 65g for a 65kg man. You would probably need 6.5g, but as Devin points out, even this dose is unlikely to hold a candle to 10mg atomexetine.Dopamine transporter inhibitory and antiparkinsonian effect of common flowering quince extract.
Zhao G1, Jiang ZH, Zheng XW, Zang SY, Guo LH. (2008)
Common flowering quince (FQ) is the fruit of Chaenomeles speciosa (Sweet) Nakai. FQ-containing cocktails have been applied to the treatment of neuralgia, migraine, and depression in traditional Chinese medicine. The present study assessed whether FQ is effective in dopamine transporter (DAT) regulation and antiparkinsonism by utilizing in vitro and in vivo assays, respectively. FQ at concentrations of 1-1000 microg/ml concentration-dependently inhibited dopamine uptake by Chinese hamster ovary (CHO) cells stably expressing DAT (D8 cells) and by synaptosomes. FQ had a slight inhibitory action on norepinephrine uptake by CHO cells expressing the norepinephrine transporter and no inhibitory effect on gamma-aminobutyric acid (GABA) uptake by CHO cells expressing GABA transporter-1 or serotonin uptake by the serotonin transporter. A viability assay showed that FQ mitigated 1-methyl-4-phenylpyridinium-induced toxicity in D8 cells. Furthermore, in behavioral studies, FQ alleviated rotational behavior in 6-hydroxydopamine-treated rats and improved deficits in endurance performance in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Furthermore, immunohistochemistry revealed that FQ markedly reduced the loss of tyrosine hydroxylase-positive neurons in the substantia nigra in MPTP-treated mice. In summary, FQ is a selective, potent DAT inhibitor and has antiparkinsonian-like effects that are mediated possibly by DAT suppression. FQ has the potential to be further developed for Parkinson's disease treatment.
Posted 27 September 2016 - 01:15 PM
And hederagenin is found in a lot of plants. I found an extract from Hedera Helix (Ivy Leaf) on eBay and an extract from Clematis Terniflora (member of buttercup family).
Tried 30mg DXM today, just slightly improved mood, no noticeable increased motivation. Tomorrow, I will try to find Ephedrine, however, it seems that Ephedrine always go with Guaifenesin. In order to take 50mg Ephedrine, I must take 800mg Guaifenesin. Is it ok to take 50mg Ephedrine and 800mg Guaifenesin if I do not have any diseases?
Posted 27 September 2016 - 04:40 PM
And hederagenin is found in a lot of plants. I found an extract from Hedera Helix (Ivy Leaf) on eBay and an extract from Clematis Terniflora (member of buttercup family).
Tried 30mg DXM today, just slightly improved mood, no noticeable increased motivation. Tomorrow, I will try to find Ephedrine, however, it seems that Ephedrine always go with Guaifenesin. In order to take 50mg Ephedrine, I must take 800mg Guaifenesin. Is it ok to take 50mg Ephedrine and 800mg Guaifenesin if I do not have any diseases?
Posted 27 September 2016 - 05:54 PM
I don't think you are going to find a nootropic magic bullet here, as much as I enjoy reading posts by devinthayer, and Gamesguru. I'm as guilty as the rest of using "research" into nootropics as a form of procrastination and a way to relieve boredom; especially since, like many here, I am easily bored, with autistic traits, comorbid anxiety, and OCD tendencies. It's hard to find a subject as engrossing, and wide ranging as nootropics!
Instead of turning inward and obsessively chronicling every little fluctuation in mood according to say, taking 30 mg of DXM, I'd encourage you to focus outward on specific goals, projects, or tasks you would like to accomplish as a measurement of your motivation.
I'm sure most of you detest positive thinking platitudes as much as I do, so I'll spare you the "a journey of a thousand miles begins with a single step" hokum, but if a life of eat, sleep, use computer, eat sleep, isn't satisfying to you, as I doubt it would be for anyone, why not make small goals of spending more time interacting socially, or just getting outside?
If you want to justify it in nootropic terms, there are few better, safer, methods of improving general and mental health that going for a walk, or jog in the countryside.
Ultimately though, I'm not sure you have a problem with motivation as much as you have a lack of direction to focus your motivation.
A vague goal of becoming "the richest man in the world" is self-defeating. How do the vast majority of the richest people in the world become rich? They are born with money. How do the others become rich? Usually, they single-mindedly pursue the creation of a product, be it a vacuum cleaner, a book, a social media company etc...without the explicit goal of vast wealth. The wealth is a byproduct. How else? Well, some people get lucky. They invest at the right time in the right company, buy real estate at the right time, or find a vast deposit of oil on their land.
Bottom line is Ephedrine/Guaifenesin, which I DO take when I have a stuffy nose, won't break the eat, computer, sleep, eat, computer cycle.
Posted 28 September 2016 - 03:59 PM
Menthol also reduces cholinergic activity. Halls has an intense cool 15mg version that is pretty effective. It does have a rebound effect with long term use, so once in a while will be fine. There are a lot of OTC anticholinergics from DXM to diphenhydramine to Bonine and NyQuil.
Guaifenesin needs to be taken with a meal and has NMDA antagonistic properties which may actually be synergistic in reducing the side effects from ephedrine. I will warn you not to use it long term like that - just for a test. It can cause kidney stones with long term use.
Tried 2.5mg Yohimbine hcl today, slightly improved mood and had more goosebumps, no noticeable increased motivation.
I could not buy Ephedrine OTC in Vietnam, they said I have to have prescription and Edephrine is usually Intravenous therapy (no oral tablets,...)
I had a story to tell you how lazy was I. Actually I had lots of motivation to do things I like, such as FIFA (ps4 game), hanging out with my girlfriend. Those things are the ones I can have fun with low effort. Today afternoon, a woman approached me and said that she picked up a mobile at a cafe. I saw and knew it was an iphone 6s, I actually could buy the iphone with a low price and sell it later, she offered selling the phone to me too, cause she had no idea what it was. Well, but think about the effort I have to use to go to the mobile stores to sell the iphone, to restore the phone, to research if the phone is locked by the owner,... I decided to refuse the offer. In conclusion, I prefer things with low effort than high effort.
Posted 28 September 2016 - 05:34 PM
Menthol also reduces cholinergic activity. Halls has an intense cool 15mg version that is pretty effective. It does have a rebound effect with long term use, so once in a while will be fine. There are a lot of OTC anticholinergics from DXM to diphenhydramine to Bonine and NyQuil.
Guaifenesin needs to be taken with a meal and has NMDA antagonistic properties which may actually be synergistic in reducing the side effects from ephedrine. I will warn you not to use it long term like that - just for a test. It can cause kidney stones with long term use.
Tried 2.5mg Yohimbine hcl today, slightly improved mood and had more goosebumps, no noticeable increased motivation.
I could not buy Ephedrine OTC in Vietnam, they said I have to have prescription and Edephrine is usually Intravenous therapy (no oral tablets,...)
I had a story to tell you how lazy was I. Actually I had lots of motivation to do things I like, such as FIFA (ps4 game), hanging out with my girlfriend. Those things are the ones I can have fun with low effort. Today afternoon, a woman approached me and said that she picked up a mobile at a cafe. I saw and knew it was an iphone 6s, I actually could buy the iphone with a low price and sell it later, she offered selling the phone to me too, cause she had no idea what it was. Well, but think about the effort I have to use to go to the mobile stores to sell the iphone, to restore the phone, to research if the phone is locked by the owner,... I decided to refuse the offer. In conclusion, I prefer things with low effort than high effort.
Posted 28 September 2016 - 05:40 PM
Menthol also reduces cholinergic activity. Halls has an intense cool 15mg version that is pretty effective. It does have a rebound effect with long term use, so once in a while will be fine. There are a lot of OTC anticholinergics from DXM to diphenhydramine to Bonine and NyQuil.
Guaifenesin needs to be taken with a meal and has NMDA antagonistic properties which may actually be synergistic in reducing the side effects from ephedrine. I will warn you not to use it long term like that - just for a test. It can cause kidney stones with long term use.
Tried 2.5mg Yohimbine hcl today, slightly improved mood and had more goosebumps, no noticeable increased motivation.
I could not buy Ephedrine OTC in Vietnam, they said I have to have prescription and Edephrine is usually Intravenous therapy (no oral tablets,...)
I had a story to tell you how lazy was I. Actually I had lots of motivation to do things I like, such as FIFA (ps4 game), hanging out with my girlfriend. Those things are the ones I can have fun with low effort. Today afternoon, a woman approached me and said that she picked up a mobile at a cafe. I saw and knew it was an iphone 6s, I actually could buy the iphone with a low price and sell it later, she offered selling the phone to me too, cause she had no idea what it was. Well, but think about the effort I have to use to go to the mobile stores to sell the iphone, to restore the phone, to research if the phone is locked by the owner,... I decided to refuse the offer. In conclusion, I prefer things with low effort than high effort.
TAAR1 agonists like ephedrine also come in nasal sprays or inhalers. What's available where you are for OTC inhalers/sprays for decongestants?
I'm sure 99% I cannot buy Ephedrine here. I went to 2 of the largest pharmacy stores, they have software which save all the drugs, medicines,... both trade names and drug names.
The guy also told me there is limited ephedrine available in my country, if hospitals want to sell them, they have to ask the government for permission, bla bla bla. In short, no ephedrine, no ritalin, no adhd.
Posted 28 September 2016 - 05:55 PM
I'm sure 99% I cannot buy Ephedrine here. I went to 2 of the largest pharmacy stores, they have software which save all the drugs, medicines,... both trade names and drug names.TAAR1 agonists like ephedrine also come in nasal sprays or inhalers. What's available where you are for OTC inhalers/sprays for decongestants?Tried 2.5mg Yohimbine hcl today, slightly improved mood and had more goosebumps, no noticeable increased motivation.Menthol also reduces cholinergic activity. Halls has an intense cool 15mg version that is pretty effective. It does have a rebound effect with long term use, so once in a while will be fine. There are a lot of OTC anticholinergics from DXM to diphenhydramine to Bonine and NyQuil.
Guaifenesin needs to be taken with a meal and has NMDA antagonistic properties which may actually be synergistic in reducing the side effects from ephedrine. I will warn you not to use it long term like that - just for a test. It can cause kidney stones with long term use.
I could not buy Ephedrine OTC in Vietnam, they said I have to have prescription and Edephrine is usually Intravenous therapy (no oral tablets,...)
I had a story to tell you how lazy was I. Actually I had lots of motivation to do things I like, such as FIFA (ps4 game), hanging out with my girlfriend. Those things are the ones I can have fun with low effort. Today afternoon, a woman approached me and said that she picked up a mobile at a cafe. I saw and knew it was an iphone 6s, I actually could buy the iphone with a low price and sell it later, she offered selling the phone to me too, cause she had no idea what it was. Well, but think about the effort I have to use to go to the mobile stores to sell the iphone, to restore the phone, to research if the phone is locked by the owner,... I decided to refuse the offer. In conclusion, I prefer things with low effort than high effort.
The guy also told me there is limited ephedrine available in my country, if hospitals want to sell them, they have to ask the government for permission, bla bla bla. In short, no ephedrine, no ritalin, no adhd.
Posted 29 September 2016 - 04:55 AM
http://www.jneurosci...ent/36/39/10002
The team found a relevant pattern of activity in three areas of the brain, the supplementary motor area (SMA), dorsal anterior cingulate cortex (dACC) and putamen. Further analysis showed that assessment of effort was centred on the SMA and putamen, with a separate network in the ventromedial prefrontal cortex assessing reward.
The dACC encoded the difference between effort and reward as a single value, likely drawing together the results of the two separate neural circuits, and activity in this area was linked with the degree to which each volunteer's choices were driven by the overall value.
Posted 01 October 2016 - 06:03 PM
Yeah but what about propylhexedrine, levomethamphetamine (which has many names, see Wiki), pseudoephedrine? Those 3 are clear TAAR1 agonists as well.
None of them available over the counter here.
How the brain decides between effort and reward https://www.scienced...60928150237.htm
http://www.jneurosci...ent/36/39/10002
The team found a relevant pattern of activity in three areas of the brain, the supplementary motor area (SMA), dorsal anterior cingulate cortex (dACC) and putamen. Further analysis showed that assessment of effort was centred on the SMA and putamen, with a separate network in the ventromedial prefrontal cortex assessing reward.
The dACC encoded the difference between effort and reward as a single value, likely drawing together the results of the two separate neural circuits, and activity in this area was linked with the degree to which each volunteer's choices were driven by the overall value.
What can I take from those studies.
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