So essentially, there’s this bill called Stop the Importation and Trafficking of Synthetic Analogues (SITSA) Act. It gives the DEA and the attorney general almost completely unchecked power to schedule any drug they see fit without following the currently established legal criteria to ban certain substances. In Section 2, Subsection 3B of the bill, this is the most worrying part that affects many different nootropics from phenibut to adrafinil or even kratom or tianepetine.
“6)Schedule A (A)In general The drug or substance—
(I)a chemical structure that is substantially similar to the chemical structure of a controlled substance in schedule I, II, III, IV, or V; and
(II)an actual or predicted stimulant, depressant, or hallucinogenic effect on the central nervous system that is substantially similar to or greater than the stimulant, depressant, or hallucinogenic effect on the central nervous system of a controlled substance in schedule I, II, III, IV, or V; and
(I)listed or otherwise included in any other schedule in this section or by regulation of the Attorney General; and
(II)with respect to a particular person, subject to an exemption that is in effect for investigational use, for that person, under section 505 of the Federal Food, Drug, and Cosmetic Act (21 U.S.C. 355) to the extent conduct with respect to such substance is pursuant to such exemption.
(B)Predicted stimulant, depressant, or hallucinogenic effect For purpose of this paragraph, a predicted stimulant, depressant, or hallucinogenic effect on the central nervous system may be based on—
(i)the chemical structure, structure activity relationships, binding receptor assays, or other relevant scientific information about the substance;
(I)the current or relative potential for abuse of the substance; and
(II)the clandestine importation, manufacture, or distribution, or diversion from legitimate channels, of the substance; or
(iii)the capacity of the substance to cause a state of dependence, including physical or psychological dependence that is similar to or greater than that of a controlled substance in schedule I, II, III, IV, or V. “
This is concerning due to Phenibut having a similar pharmaceutical effect to Lyrica (schedule V) nd also being able to be (A) abused, and (B) can cause addiction or dependence similar to benzodiazepines or other GABApentinoids.
Adrafinil is an analogue of Modafinil, a schedule IV drug, so it’s obvious why that could be banned immediately.
Here is the link to the whole bill’s information, contact your reps, we need to stop this bill.
Edit: there’s a letter from Human Rights Watch to Congress concerning this for those interested: https://www.hrw.org/news/2018/06/14/opposition-letter-hr-2851-stop-importation-and-trafficking-synthetic-analogues-sitsa
I believe taking Chamomile and Lemon Balm together has a synergy.
Chamomile contains a flavonoid called Apigenin. Apigenin binds to the GABA-A receptors.
Lemon Balm has been known to prevent the breakdown of GABA by inhibiting enzymes that break it down. However, it is unknown whether Lemon Balm will break down the effects of Apigenin.
I have been taken tea of Chamomile and Lemon Balm -- both seperate and together. My personal conclusion is that while Lemon Balm does make the anxiolytic and relaxing effects from Chamomile more potent it also increased the duration. The effects have enhanced my ability to plan things out as well as the ability to "take a step back". If it were to be compared to a moderate dose of Alprazolam on a scale of 1 to 10 -- it would be a 5 out of 10.
The only concern is tolerance and withdrawal for Lemon Balm. I believe that Chamomile, on the other hand, does not have any withdrawal and tolerance. I have yet to experience any negative effects from Lemon Balm, however it is expected.
As for the route of administration, I took both Chamomile and Lemon Balm via tea and vaporization. Tea is the preferred method as you'll get the full effects for longer.
For tea: Heat water to a boil (212 F / 100 C). Let it steep for however long you want. The longer the better -- anything after 25 minutes you're not going to get any stronger effects. After ingestion, the full effects will show up within 10 to 30 minutes. YMMV.
For vape: Chamomile vaporizes at 190 C. Lemon Balm vaporizes at 130 C. You're going to want to start inhaling when the temperature reaches 130 C and continue to inhale until it reaches 190 C. You may set the temperature 3 degrees higher than 190 C if you'd like. The full effects will show in under 5 to 10 minutes.
You may add Lavender into the blend for a better sleep aid, however, this may be overdoing it.
From "Handbook of psychopharmacology Volume 20 Psychopharmacology of the Aging System"
Recently expressed ideas, developed mainly at the Massachusetts Institute of Technology, argue that nootropic drugs may be contraindicated in Alzheimer's disease unless concurrent supplemental doses of choline (or lecithin) are given. Since these ideas are now current and provide new perspectives on this class of drugs, they require discussion here. The basic starting point for these ideas is the fundamental observation that the level of choline inside a cholinergic neuron is important to its function, and that rapid firing of the neuron tends to deplete this internal level of choline (Parducz, 1984). The internal depletion of choline would naturally be most severe when the neuron is firing rapidly and/or when the supply of extracellular choline is low. The Massachusetts Institute of Technology group goes on to suggest that the cholinergic neuron is unique in that it can break down its own membrane to obtain the needed choline when the extracellular supply of choline is inadequate. Thus, the cholinergic neuron utilizes phosphatidylcholine not only as a membrane constituent, as other neurons do, but also as a reservoir of free choline for transmitter synthesis (Blusztajn ('[ at., 1984). However, this "autocannibalistic" process can lead to the death of the cell if carried too far. The death of the cell would be most likely to occur when the extracellular level of choline is low and when the neuron's firing rate is high. Therefore,456 B. P. H. POSCHEL under these conditions supplemental doses of choline in the diet should have value. The original use of choline in treating Alzheimer's disease was based solely on the notion that greater availability of choline would increase the amount of transmitter formed in, and released from, still functioning cholinergic neurons. And it now seems confirmed that increased plasma choline does indeed augment the amount of acetylcholine released from frequently firing cholinergic neurons (Blusztajn and Wurtman, 1983). But now the further idea is proposed that supplemental choline in Alzheimer's disease could have the additional benefit of reducing the amount of autocannibalism. Therefore, even if choline supplements do not have a rapid and direct effect on Alzheimer symptoms, they could limit or retard the progress of the disease. Unfortunately, it would be difficult and expensive to prove this point in patients because long-term trials would be needed. A corollary of these ideas is that administration of a nootropic drug without choline to patients with Alzheimer's disease may be harmful in the long run. Tp.is conclusion is suggested by the fact that a drug such as piracetam is believed to enhance the firing rate of cholinergic neurons (Wurtman et at., 1981). The single-neuron effects we presented in this chapter strongly indicate that pramiracetam also has this action on firing rate, only more strongly. Thus, while the increased firing of cholinergic neurons could have an immediate beneficial effect in Alzheimer patients, the long-term effects could be harmful because autocannibalism might be augmented. However, administration of choline as a food supplement along with the nootropic drug treatment could theoretically avoid the longterm harmful effect entirely. These interesting ideas have, of course, yet to be tested clinically. The choline-nootropic drug combination has been studied also for a different reason, namely, in the hope of discovering an immediate synergistic facilitatory action between the agents on learning and memory. In one study employing aged rats a large synergistic effect on passive avoidance was observed after 100 mg/kg of piracetam and 100 mg/kg of choline were administered for 1 week (Bartus et at., 1981). Another study employed young adult mice and found a large synergistic effect on habituation of exploratory activity after 50 mg/kg of both piracetam and choline were administered, only once, immediately after the acquisition session (platel et at., 1984). In this study the synergistic effect on learning and memory appeared to depend on using just the right dose of both agents. Thus, the findings were suggestive of a therapeutic window, although the authors did not discuss their data from this point of view. In addition, an exploratory study on memory performance of human senile demented patients treated with this drug combination has been conducted (Ferris et at., 1982). A favorable effect on memory in some of the patients was reported, and this effect was considerably larger than previously seen with choline treatment or piracetam treatment alone.NEW PHARMACOLOGICAL PERSPECTIVES ON NOOTROPIC DRUGS 457 Further work combining choline with nootropic drugs appears to be warranted. The approach is promising for theoretical reasons and because of empirical findings obtained to date. However, judging from the Platel et at. (1984) study conducted in mice, selecting the very best dose of either agent to treat a particular patient could be a problem. This factor may conceivably help to explain why in the Ferris et at. (1982) study the majority of the patients did not clearly improve clinically
During the week, I get anywhere from 4-7 hours of sleep, depending on the day. Usually I'm feeling pretty good at work, even on little sleep, and have a decent amount of energy and mental ability. However, on most weekends I can sleep 8-10 hours, get out of bed, and feel nothing but mentally foggy, tired, anti-social, and my attention span decreases significantly.
Really the only difference between Friday and Saturday is about 2-3 hours of extra sleep. Yet those extra 2-3 hours completely shut down my entire day. I feel straight up stupid, unable to concentrate on anything, all day long after 8+ hours of sleep. I literally feel like I'm 50% mental capacity. Caffeine actually worsens the problem on weekends, whereas it's somewhat helpful to me during the week.
This has been going on for a few months now. Any ideas on why more sleep negatively affects my cognitive abilities? And as a side question, are there any nootropics that are mildly or totally non-stimulating, but work well as a "day starter?"
I was just wondering if I go on a flight and I try to bring my nootropics (literally my medication), will I have to do anything special with them? I would hate for someone to mistake them as cocaine or meth or something. It's literally piracetam, pramiracetam, and alpha gpc.
First off, yes Iv done a bunch of research on nootropics and various drugs but I very much respect this subs knowledge. On paper, doing only welbutrin on the weekends, and using nicotine on weekdays kinda sounds like it could work to prevent tolerance, and the welbutrin on the weekends could help reduce cravings. But it wouldn't build up as to negate the effects of weekday nicotine use.
Hello! It's my first time posting here, but I've been a lurker for a while. :)
I bought some Ashwagandha root powder capsules. I took two per day (amounts to 1200mg total), one with lunch and one with dinner. I noticed a slight decrease in stress after doing this for about a week, but the effects were never very prolonged. Just in case I was missing something, I decided to keep trying them.
One night, I realized I had forgotten to take any Ashwagandha that day and I decided to take both pills before bed. The effects were much more pronounced. So much that I decided to continue it for a few weeks. These were the results:
I don't believe Ash is a miracle supplement, but it has definitely helped me with the above. Anyone have any tips/similar experiences?
Edit: Since this is getting some attention, I want to echo this thread: Ash + alcohol = bad hangovers. :) Also, /u/Blubah78 said Ash was a gaba agonist and that users should be careful of dependence. I have not experienced any symptoms, but it's good to know.
Almost every positive post I see here is someone clearly in a manic state according to some people, so my question is how can you tell a truly positive experience from a manic/hypomanic state? I don’t want to start a stack, have what I perceive to be a great experience only to find out it was only mania.
There are a lot of love stories with lsd on the microdosing sub; it’s really a big circle jerk, but I guess that’s how it is with all specialty subs. I’ve been playing around with microdosing 1p lsd for nootropics purposes, mostly for a change of perspective, and it’s work in progress but kind of underwhelming as of now. So who else has tried this and for what purpose and how is it really? I’ve asked in the microdosing sub, but I want to ask here for more objective responses.
Many people say it's a dangerous supplement, but this link Mucuna pruriens (Examine.com) mentions a study where infertile men used 5g per day for three months. I don't have infertility problems (I take it for nootropic purposes), but in this study there were healthy men as controls who also took 5g. Does this imply that 5g is okay?
Examine.com also says "One large double blind study noted no significant adverse effects from 15-30g of Mucuna Pruriens powder over the course of 12-20 weeks aside from one patient suffering from vomiting, which was deemed unrelated to the bioactivity of Mucuna but rather its digestability and palatability." Although they were Parkinson's disease patients, this could probably mean that high doses like 15g is safe.
I've been taking 4.8g for two days and think the results are subtle. I'll keep on but would like some opinions about this.
Read my old threads. I tried almost everything except modafinil, adderall, nsi-189. They can't be bought in my country.
Best helps: running and a good sleep. The diet didn't have any effect.
Now I run every day for half an hour and another half hour or an hour walk.
My only question is: why didn't I start doing this before?
I, like many others, didn't believe in the effect of the running.
Don't be afraid to start, for the first weeks I was choking from 1 minute of running, now I run better than all my friends.
The effect of euphoria and increased mood reminds me of the high dosages of bromantane with piracetam and uridine. But running gives energy, removes brain foog, raises the mood for the whole day and the next one too. Memory also became much better. And the tablets quickly provoked tolerance. Running has no tolerance.
Now I only take piracetam and eat eggs for breakfast. Running replaces all other nootropics.
I took 700mg of pramiracetam (Nootropicsdepot, so no contamination/impurities), and 2 hours later, couldn't think straight, trouble with expressing emotions, and profound irritability. The cognitive impairment is Soo bad, I am still feeling remaments of it. I just want to go to sleep type of feeling. How long will this side effect last?
Not taking any other nootropics except for a the last couple of weeks, 500mg of CDP choline.
P.S. still having trouble with deep/higher order thinking skills. Do I have possible permament brain damage do to nitric oxide synthase? I thought that doesn't happen if you go pass 1,012 grams in humans? Still feel the effects but not too bad. Should I go back on CDP choline to relieve the build up of nitric oxide due to CDP choline on gluthaione?
Has anyone else noticed this? I contacted them and haven't heard back. I went to go order and it doesn't appear to be an option as it always has previously
I was researching it on pubchem because it's in just about every nootropic or supplement. I discovered this info on toxicity
I research compounds all the time on here. I have never seen this much toxicity data, especially for such a commonly used compound.
There are over 20 points of data indicating a tumorigenic quality in living species.
There are over 50 reports documenting a low toxic dosage.
There are 8 reports of Dna mutation occurring from its usage
All of these reports are in living beings. Some are in HUMANS
Why is this compound so frequently used? It doesn't even do anything except fill, and prevent caking.
These aren't even qualities we desire. We don't want silicon dioxide powder. And we don't want silicon dioxide capsules. But its cheap, makes stuff a lot easier to handle on the production line due to its anti caking, and it makes capsules look more full.
Is this another case of "well yeah its poison but youre only get a little every day so don't worry about it"?
For comparison here's another extremely common filler, magnesium stearate https://pubchem.ncbi.nlm.nih.gov/compound/magnesium_stearate#section=Toxicity&fullscreen=true
Note there's only 3 studies, probably because the first few ones they did found it had an unachievablely high toxicity dose more in line with "natural" substances