Thought I would share something of personal interest to me.

If you guys want to contribute stuff you know, feel free! Adderall is a 75/25 split between D-amphetamine and L-amphetamine (containing 4 different salts, two of which are purely D-isomer, the other two being racemic amphetamine). D-amphetamine is the psychoactive component of Adderall (and Dexedrine), functioning on the mesolimbic reward pathway in the brain to increase ambient dopamine and norepinephrine levels in the brain tissue. Dextroamphetamine (amphetamine meaning alpha-methylated phenethylamine) mimicks dopamine (an endogenous neurotransmitter and phenethylamine) and norepinephrine (ditto) in the brain, binding to the reuptake channels in the synapse and blocking reuptake by essentially clogging the pathway and being hard to immediately metabolize and remove. Thus, dextroamphetamine acts as a norepinephrine-dopamine reuptake inhibitor (an NDRI, the same class of drug as Wellbutrin). Increased ambient levels of dopamine in the mesolimbic reward pathway, where dopamine normally functions as your "learning" neurotransmitter, increases motivation and focus. The norepinephrine provides the wakeful effects of the drug, as norepinephrine is the primary metabolite of epinephrine, or more commonly, adrenaline. Adrenaline acts directly on the peripheral nervous system, but must be metabolized into norepinephrine to cross the bloodbrain barrier and function centrally. Levoamphetamine is a weak stimulant that promotes wakefulness and can cause discomfort in some users. It has a longer metabolization half-life than dextroamphetamine, and subjectively lessens the effects of amphetamine comedown in some users. Anonymous 06/04/11(Sat)04:29:21 No.332181483 File1307176161.png-(5 KB, 448x221, mdma.png) MDMA (3,4-methylenedioxymethamphetamine), more commonly known as ecstasy, is an empathogenic (to cause empathy)/entactogenic (to touch within) stimulant of the amphetamine family. Though a phenethylamine, the two-ring structure mimicks the structure of a tryptamine (an amine with the two-ring structure of the amino acid tryptophan), and as such, instead of functioning on the mesolimbic reward pathway typical of amphetamines, MDMA functions in the serotonin pathways of the brain. Like dextroamphetamine, MDMA is a reuptake inhibitor (a serotonin-selective reuptake inhibitor, or SSRI), and also reverses the function of the reuptake inhibitor, raising ambient levels of serotonin dramatically. Subjectively, MDMA causes intense feelings of pleasure and empathy, typical of serotonin (the "feel-good" neurotransmitter).

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>> Anonymous 06/04/11(Sat)04:30:02 No.332181563 >>332181483 MDMA interacts with a number of anti-depressant medications. SSRI class medications (Prozac etc.) suppress the functioning of MDMA. Most therapeutic SSRIs

have a very high binding affinity mu, which means when they bind to the reuptake channels in the brain, they are very hard to metabolize and remove. MDMA's mu, comparably, is quite low, and as such, it cannot bind to the serotonin receptors in your brain effectively, and as such, has no effect. MAOI class antidepressents have a fatal counterindication with MDMA. MAOI stands for monoamine oxidase inhibitor, which means that they block the enzymes which break down monoamines (serotonin and dopamine) in the brain. When MDMA binds to a reuptake channel and begins secreting serotonin into the synaptic cleft, the serotonin cannot be broken down, and since it cannot be reuptook, it continually triggers the dendrites of the neighboring neuron, resulting in overstimulation and a dangerous event known as "serotonin syndrome". Serotonin syndrome, also "serotonin toxicity", is essentially having too much serotonin in your brain at any one time, and results in extreme vasoconstriction, which impedes blood flow to your organs. Don't take MDMA if you're on an MAOI! Wellbutrin (an NDRI) potentiates MDMA, but increases the likelihood of seizing while on many drugs, most specifically stimulants. Anonymous 06/04/11(Sat)04:42:27 No.332183018 File1307176947.jpg-(35 KB, 483x604, beer.jpg) Alcohol (ethanol or ethyl alcohol) is a depressant type drug, functioning primarily by binding to GABA receptors in the brain. Gamma aminobutyric acid (a gamma amino acid, with the amino group bound to the third carbon - fourth counting the carboxyl group, hence, "butyric") is a neurotransmitter which causes hyperpolarization of neurons by forcibly opening the ion channels of the axon. A hyperpolarized neuron cannot fire its action potential, and is thusly inhibited - alcohol is a central nervous system depressant that functions by inhibiting the firing of neurons. >> It acts from the top down, or from the more highly developed areas of the brain toward the less as your BAC increases. The "top" level of the brain, the precortex, is the area of your brain involved in forethought, cause/effect, value assessment, etc. When you begin drinking, you are disinhibited, and don't care about the consequences of your actions. Alcohol then moves to the cerebellum, inhibiting balance and coordination. On its way there, it passes through the temporal lobe, where fine motor skills and the speech centers are located. It then moves down into the hippocampus, which converts short term memories into long term memories, and then into the brain stem, which controls your unconscious functions such as breathing. That's why when you drink alcohol, you're first socially disinhibited, then become clumsy, forget what happened, and ultimately pass out and/or die. Careful with alcohol, it's very dangerous! >> Anonymous 06/04/11(Sat)04:47:40 No.332183633 >>332183018

Alcohol functions similarly to benzodiazepines (Xanax, Klonopin, etc.), and long term usage can lead to physical dependency. Alcoholism, and benzodiazepine withdrawal, is caused by an ambient decrease in GABA. Since GABA is involved in inhibiting neurons, a of GABA causes symptoms such as neural pain, tremors, seizures, and even death! Alcohol and benzodiazepine withdrawal can be FATAL, so if you're an addict, NEVER go cold turkey on either. Always, always, always taper. While alcohol tapering can be done simply by drinking less, benzodiazepine withdrawal is a bit more tricky. The currently accepted method is a switch over to an equivalent dosage of Valium (diazepine), which untypical of benzodiazepines, has a comparably high dosage threshold (tens of milligrams instead of single digit doses). From there, a percentage decrease in dose every two weeks or so is suggested until you are completely off. If you are experiencing discomfort when switching to a lower dose, don't push it. Return to your last comfortable dose, and try again in another two weeks. The more uncomfortable the withdrawal symptoms are, the more likely relapse is, so take it slow and steady. Anonymous 06/04/11(Sat)05:01:10 No.332185105 File1307178070.jpg-(45 KB, 600x450, weed.jpg) Marijuana's active ingredients are all cannabinoids, notably delta-9-tetrahydrocannabinol (THC), as well as cannabidol (CBD), cannabinol (CBN), and others. Cannabinoids mimick anandamide in the body, the endogenous cannabinoid in humans. Anandamide is derived from arachidonic acid, which is an important peripheral neurotransmitter in its role in causing inflammation and pain. Increased levels of cannabinoids decrease the speed at which enzymes that metabolize arachidonic acid can function, which is one of the primary causes of marijuana's pain-suppressing abilities. Cannabinoids function centrally by binding to cannabinoid receptors 1 (CB1) and 2 (CB2). The endogenous cannabinoid system plays an role in the depolarization of neurons (functionally the opposite of GABA), which allows neurons to repolarize and fire again. Thus, cannabinoids allow for the more rapid firing of neurons in the brain, suppressing inhibition of neurons. Ever notice how your thoughts race and become more vivid when high? Cannabinoid receptors are very common in the temporal lobe, which contains areas such as the hippocampus (memory formation), the amygdala (fear), and various sensory-related parts of the brain. This all explains why, when high, it becomes easier to forget things, easier to become paranoid, and sensation is generally more vivid. Anonymous 06/04/11(Sat)05:03:14 No.332185333 >> wart

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>> Anonymous 06/04/11(Sat)05:13:10 No.332186418

umm..... archive this shit? OP is not a fag. It would appear that he has dropped some knowledge upon us. Thanks OP! Anonymous 06/04/11(Sat)05:13:44 No.332186478 File1307178824.jpg-(71 KB, 500x418, aspirin.jpg) On the note of pain and arachidonic acid, let's take a bit of a detour into the world of Aspirin (acetylsalicylic acid) and other NSAIDs, or non-steroidal anti-inflammatory drugs. Arachidonic acid, as previously stated, plays an important role in the expression of pain and inflammation. Arachidonic acid is metabolized by cyclooxygenase (COX, in varieties 1 and 2). Cyclooxygenase is irreversibly inactivated by salicylic acid, most of which is formed endogenously. Salicylic acid is rapidly decomposed in the acidic environment of the stomach, but by attaching an acetyl group by synthesizing salicylic acid with acetic anhydride, the newly formed acetylsalicylic acid can endure the proton concentration of the stomach and move into the small intestine to be taken up into the bloodstream. There, the acetyl group dissociates from the salicylic acid, wherein the salicylic acid inhibits the cyclooxygenase, and fends off pain and inflammation. As previously stated, cyclooxygenase comes in two varieties, COX-1 and COX-2, each being involved in different processes. While COX-2 is the isozyme related to pain and inflammation, COX-1 is involved in platelets forming into clots and scabs. Typical OTC NSAIDs (Aspirin, Ibuprofen, Tylenol) are nonselective, and as such have the unintended side-effect of thinning the blood. While this can be beneficial for hypertensive patients at threat for blood clots, it can also cause stomach ulcers and internal bleeding. The search for a COX-2 selective inhibitor was a big deal in the pharmaceutical industry, and some headway has been made with drugs such as Celebrex and Vioxx. Unfortunately, these two drugs have other side-effects (notably carcinogenic), and as such, have been recalled from the market, leaving chronic pain patients in a poor situation. Anonymous 06/04/11(Sat)05:17:12 No.332186898 >> seriously my friends don't understand why i love learning about drugs but i think that the science behind why i feel crazy when i pop a couple molly is outstanding. thanks for being awesome op Anonymous 06/04/11(Sat)05:18:25 No.332187043 >> reading up on the pills mommy gets you, huh

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Anonymous 06/04/11(Sat)05:31:56 No.332188523 File1307179916.jpg-(57 KB, 600x776, heroin.jpg) While still on the topic of pain, and back to psychoactives/centrally acting drugs, heroin, morphine, oxycodone, and all other opiates work as such: there are three primary opioid receptors in your brain, of delta, kappa, and mu varieties. All three are involved in your typical opiate functions: analgesia, sedation, pupil constriction, respiratory depression, etc. They are activated endogenously by your endorphins (endorphin meaning "endogenous morphine"), those feel-good drugs considered responsible for a runner's high, the euphoria following intense physical exertion - though evidence has shown that the endocannabinoid system plays a role in this as well. Anyway, once in your blood, these opiates flood your brain and bind to your opioid receptors. Some opiates, like codeine, are inactive prodrugs (to the first post, Vyvanse is lisdexamphetamine, a prodrug for dextroamphetamine) that are metabolized into morphine in the body. These opiates are receptor agonists, binding to receptors and triggering their function. Once triggered, these opiates release a flood of neurotransmitters into the brain, primarily in the central regions and the spinal cord/brain stem. This causes an intense euphoria, and depresses certain lower brain functions such as respiration and wakefulness. Anonymous 06/04/11(Sat)05:33:21 No.332188693 >>332188523 Morphine, being the primary component of opium (and the drug that codeine, the secondary component, metabolizes into), is considered the "baseline" for opioid strength comparisons. While certain opioids have different affinities for the three opiate receptors, they all function in a fairly similar way. Oxycodone (Oxycontin) is approximately twice as strong as Morphine. Hydromorphone (Diladuid) is about five times as strong, and oxymorphone (Opana) is in the realm of seven or eight. Heroin (diacetylmorphine) is about four and a half times as strong. There are many opiates, some being ludicrously strong. Fentanyl, often prescribed for cancer patients, is around 100 times stronger than orally taken morphine. Alpha-methylfentanyl, known as China White, is of similar strength, while 3-methylfentanyl is around five thousand times stronger than morphine. It's crazy how much a simple CH3 can alter the strength of a drug (again, back to the first post: compare methamphetamine to dextroamphetamine). >>332187043 I'm a biochemistry major, drugs have always fascinated me. If you guys have anything cool/interesting you want to share, drug related or not, feel free to share! Learning stuff like this is awesome for me, and the topic is nearly irrelevant.

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Anonymous 06/04/11(Sat)05:37:27 No.332189108 >> Hi OP, can you explain the difference between "meth" and "speed"? Anonymous 06/04/11(Sat)05:40:36 No.332189477 >>332188693 >biochemistry fuck that shit Anonymous 06/04/11(Sat)05:47:57 No.332190299 File1307180877.jpg-(67 KB, 500x375, psychedelic.jpg) Anyway, here come some info on psychedelics. Psychedelics (mostly tryptamines like psilocybin, and some phenethylamines like mescaline) are serotoninergic drugs which function as 5-HT2A agonists (5-HT, or 5hydroxytryptamine, is the scientific name for serotonin). This very specific receptor, a subset of the 5-HT2 receptor group (which is further a subgroup of all 5-HT receptors), prevalent mostly in places such as the visual cortex and the orbitofrontal cortex. The orbitofrontal cortex an area of the prefrontal cortex and unfortunately is poorly understood, but the current theory is that the area is involved in the integration of senses, and how these sensations are used in decision making. In relation to psychedelics, this would potentially explain the synesthesia (blending of senses, e.g. "hearing color") and strange thought-loops associated with psychedelics. Damage to the region is known to cause an inability to empathize and poor social interaction, which runs counter to the entactogenic effects of many psychedelics. As far as the visual cortex is concerned, well, duh! Psychedelics make you see shit! Your typical psychedelics (LSD, psilocin, mescaline) are what are known as inverse agonists of the 5-HT2A receptor. Inverse agonists are agonists, compounds which bind to a receptor and induce some function, but produce the opposite of the typical biological reaction. This results not only in the inhibition of the typical neurological response, but produces effects beyond nothing, or a negative effect. The reversal of typical functions in the visual and orbitofrontal cortex explains why areas that are regularly used to observe, classify, and understand sensations go haywire. >> Anonymous 06/04/11(Sat)05:50:47 No.332190598 >>332186418 You could find this on wikipedia. It's probably

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copypasta. Anonymous 06/04/11(Sat)06:08:13 No.332192417 File1307182093.jpg-(15 KB, 250x386, nice haircut.jpg) >>332189108 Speed typically refers to (dextro)amphetamine, which is a potent CNS stimulant. (Dextro)methamphetamine is derived from amphetamine and instead of ending in NH2, that amino group is methylated and the drug ends in NH-CH3. This increases the drug's solubility in brain tissue, and as a result, causes a much higher peak in dopamine/norepinephrine levels in the brain as compared to dextroamphetamine. This also might explain why dextromethamphetamine is so much more neurotoxic than dextroamphetamine. Cool fact: levomethamphetamine is not centrally active, and as a minor stimulant, is used in products such as Vick's nasal spray to open up the sinuses. Anyone ever heard of the phantom cigarette? It's a strange phenomena that occurs when people have been using a class of hallucinogens known as deliriants (with such fun drugs as diphenhydramine, AKA Benadryl, datura, nutmeg...) where the user will smoke a cigarette that isn't there. It's a really common thing, too, and there's a reason for it: deliriants function as anticholinergics. Acetylcholine, another neurotransmitter, is best known as the neurotransmitter which transmits nerve impulses in muscles. When you have too much (Sarin, a nerve gas, functions by inhibiting cholinesterase), all of your muscles contract, you're paralyzed, and you asphyxiate to death. Too little (caused by Tabin & co.) makes your muscles not work, you shit yourself, and then you asphyxiate to death. >> Anonymous 06/04/11(Sat)06:09:48 No.332192577 >>332192417 Luckily, deliriants don't act very strongly on the peripheral nervous system, or they would be deadly. Instead, they act centrally, where acetylcholine is a neuromodulator important in synaptic placticity (the ability for impulses to change in strength) and long-term potentiation (the ability for a neuron to fire off a continuous signal for an extended period). These things are important for memory, and in the parasympathetic nervous system, controlling involuntary movement. When you've taken a lot of an anticholinergic, you twitch uncontrollably and hallucinate to see things that aren't there. So how is this related to the phantom cigarette? Nicotine's central function is as a

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cholinergic, triggering nicotinic acetylcholine receptors in the brain. Your brain wants a cigarette because it doesn't have enough acetylcholine, and cigarettes cause a central release of acetylcholine. Since you imagine things are there while delirious, hey! Here's a cigarette! Let's smoke it. Most deliriants are antimuscarics, meaning they block muscaric acetylcholine receptors. Nicotinic acetylcholine receptors are unaffected, so if you're ever freaking out on deliriants, smoke a few cigarettes and you'll probably feel better. >>332190598 I'll admit to looking up Wikipedia for the vocabulary (no way in hell I would have remembered "muscaric acetylcholine receptors"), but most of this is what I've known. Granted, it's not the most in-depth stuff, but if it piques anyone's interest, I'll discuss more. Maybe I'll get a few other people interested in psychopharmacology, the academic love of my life. Anonymous 06/04/11(Sat)06:11:54 No.332192807 File1307182314.jpg-(246 KB, 962x711, 1277737127992.jpg) >> Sweet, a drug info thread. >> Anonymous 06/04/11(Sat)06:11:59 No.332192814 File1307182319.jpg-(294 KB, 1619x1578, 1304745630459.jpg) Anonymous 06/04/11(Sat)06:20:01 No.332193658 File1307182801.jpg-(1.22 MB, 1484x998, Pill Guide.jpg) Can you explain whats the difference between : >> >Adderall with the combination of 75% Dextroamp & 25% Levoamp >And the pure dexamp Which is better in some given situations? Anonymous 06/04/11(Sat)06:22:46 No.332193937 File1307182966.gif-(35 KB, 564x600, 1277732112992.gif) >> Anonymous 06/04/11(Sat)06:28:37 No.332194576 File1307183317.png-(232 KB, 1080x763, 1279284007860.png) >>332193658

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Never mind. I see you explained it already, lol. Anonymous 06/04/11(Sat)06:29:33 No.332194672 >>332193658 Dexedrine, pure dextroamphetamine, has a higher peak plasma concentration per equivalent dosage, wears off faster, and generally allows you to sleep about 10 hours after taking it. Subjectively, it has a nasty crash at the end. Take it if you want the concentration/focus factor of the amphetamines, but not the prolonged uppiness. >> Adderall has a lower peak plasma concentration comparable to Dexedrine, but the effects last longer, and the comedown is more gradual. It's also prolonged, and while levoamphetamine won't give you the concentration of dextroamphetamine, it will keep you up. Take it if you don't need to sleep for a while, and/or want to avoid the amphetamine crash. They both have their pluses and their minuses. I caution against taking either multiple days in a row (always try to keep an off day if you can), because the biggest immediate danger in amphetamine usage is sleep deprivation. Once you crack the 48 hour mark and start heading toward 72 hours, you generally start to get delirious and enter a psychotic state. Anonymous 06/04/11(Sat)06:30:50 No.332194812 File1307183450.png-(374 KB, 700x2500, 1277464324016.png) >> Anonymous 06/04/11(Sat)06:33:52 No.332195133 File1307183632.jpg-(87 KB, 600x840, 1279289667860.jpg) >>332194672 Thanks, that cleared up many things. >> Anonymous 06/04/11(Sat)06:35:13 No.332195261 >>332195133 No prob. Anonymous 06/04/11(Sat)06:35:30 No.332195291 File1307183730.jpg-(850 KB, 1024x3000, 1277482520498.jpg)

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Anonymous 06/04/11(Sat)06:37:39 No.332195502 File1307183859.png-(49 KB, 460x1046, 1280527951061.png) >> Anonymous 06/04/11(Sat)06:40:41 No.332195800 a neat trick i learned to make adderall stronger and last twice as long is to swallow a spoonfull of baking soda 30 mins before taking it something to do with making it more difficult to excrete amphetamines from your bloodstream Anonymous 06/04/11(Sat)06:41:25 No.332195866 >>332195261 Also, there's Vyvannse (lisdexamphetamine), a prodrug which is essentially a lysine tacked onto the amine group of the amphetamine. It's inactive until pepsin in the stomach cleaves the lysine off, so it can only be taken orally (sorry, tweakers), but has benefits of both Dexedrine and Adderall. Since the drug has to first be metabolized, there is a longer duration of effects compared to Dexedrine, but shorter than that of Adderall as it contains no levoamphetamine. It offers a longer duration without the sustained wakefulness of Adderall - unfortunately, Vyvanse has the lowest peak concentration of all three drugs, and still has the Dexedrine crash. Methylphenidate (Ritalin/Concerta) is some weirdo thing that isn't an amphetamine. Similar function, though. Anonymous 06/04/11(Sat)06:41:52 No.332195915 File1307184112.png-(500 KB, 860x1290, 1280528222061.png) >> Anonymous 06/04/11(Sat)06:45:31 No.332196278 How do I lessen the crash when coming off adderall? I get crazy mood swings and want to cry. > Anonymous 06/04/11(Sat)06:45:50 No.332196315 > >>332195800 hey guess what happens when the baking soda reacts with the strong acids in your stomach? very funny kiddo

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>> Anonymous 06/04/11(Sat)06:45:55 No.332196325 >>332195800 Lower stomach pH increases absorption of amphetamines. taking antacids and low pH

substances (milk) can lower stomach pH. Acidic foods and vitamin C fruit drinks will make stomach pH high and less absorption will take place. Anonymous 06/04/11(Sat)06:47:10 No.332196494 >> >>332196325 PROTIP: EATING BAKING SODA WILL MAKE YOU BURP UNCONTROLLABLY LIKE A MOTHERFUCKER Anonymous 06/04/11(Sat)06:47:33 No.332196537 >>332195800 Baking soda is a basic agent, and raises the pH of the stomach. The higher the pH, the less effective your pepsin is. The less effective your pepsin, the less amino acids you have being deaminated. The less amino acids you have being deaminated, the less urea you produce. The less urea you produce, the less you'll need to pee. Essentially, instead of getting to the kidney and being excreted, the amphetamine will continue to circulate in your blood since you aren't passing as much fluid through those nephrons. Nearly a full half of amphetamine is excreted renally and intact, so the less you pee, the more you got in your blood. Won't last forever, though, your liver will eventually metabolize it. Anonymous 06/04/11(Sat)06:51:35 No.332196985 >>332196537 >> an idea what the long term effects are? am i basically destroying my body by doing this? Anonymous 06/04/11(Sat)06:52:11 No.332197044 File1307184731.jpg-(711 KB, 1053x588, 1277212427907.jpg) >> Anonymous 06/04/11(Sat)07:00:15 No.332197921 File1307185215.jpg-(410 KB, 1920x1003, Picture-1.jpg) Haha > Anonymous 06/04/11(Sat)07:03:40 No.332198300 > >>332196537 i take dexedrine for add and narcolepsy but i like to have a

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fresh apple and carrot juice in the morning does the change in ph effect the performance of the drug because i notice it doesnt have much of an effect if i have it with it and that i need to take a larger dose Anonymous 06/04/11(Sat)07:07:30 No.332198720 >>332196985 Long term basification of the stomach can cause stomach ulcers. It's a problem in people who chomp on antacids all the time - they cause damage to their stomach lining, which is meant to function in low pH environments, and get ulcers. When they feel stomach pain coming on, they eat a few antacids, and make the situation worse. It's also bad for your digestion in general, since pepsin in your stomach misfold at higher pH ranges, and a good way to get food poisoning, as the stomach's pH helps kill incoming bacteria. Is it gonna kill you if you mack on a bit of baking soda every now and again? Probably not. Still, if you do it regularly for an extended period, that's where you'll run into problems. Anonymous 06/04/11(Sat)07:10:45 No.332199030 File1307185845.jpg-(731 KB, 810x3000, 1274865264489.jpg) >> Anonymous 06/04/11(Sat)07:12:21 No.332199168 >>332198300 The effect would be minor. Apple juice is acidic, sure, but not so much as your stomach acid already is. The reason the baking soda thing does what it does is because the alkaline baking soda interferes with pepsin's folding. Unless you're drinking HF or a superacid, your stomach's pH isn't gonna go low enough to denature your digestive enzymes. More likely than not, you're just developing a tolerance with a daily dose. Try to take it only on days when you're absolutely gonna need it (if you're spending the day at home, your narcolepsy won't be a huge issue), as it'll keep your tolerance low, and it's probably better for your body. Also, I dunno if you do or not, but make sure you exercise regularly and eat healthy, that does wonders for most minor to moderate sleep disorders. Anonymous 06/04/11(Sat)07:15:09 No.332199440 >> >>332192814 lol'd

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>> Anonymous 06/04/11(Sat)07:16:10 No.332199542

pure dextro is much better than adderall. Anonymous 06/04/11(Sat)07:19:41 No.332199900 >>332199168 yea im at 15% body fat and i eat healthy try not to skip meals and i go to the gym 2 - 3 times a week (mostly thanks to taking the dex because im super lazy if i don't) my sleep disorder has gone away now i mostly take it for the add and go to uni full time >> but I often go out partying and take about 10mg at the start at the night and then again later for confidence and to be more sociable but i often end up drinking too... how dangerous is this? i mean to stop but i really enjoy life doing this and what i would do before is sit at home browsing newt gingrich and playing vidya every friday night with no friends Anonymous 06/04/11(Sat)07:21:51 No.332200163 >> >>332199168 wait is orange juice a super acid because i often have a glass of orange juice or breakfast juice as well (i drink a lot of water and liquids during the day atleast 1-2 litres, never soft drink and almost exclusively sparkling mineral water) Anonymous 06/04/11(Sat)07:24:40 No.332200478 File1307186680.jpg-(496 KB, 500x3575, 1279355548727.jpg) >> Do you know anything on decreasing tolerance like magnesium tablets? >> Anonymous 06/04/11(Sat)07:25:11 No.332200529 Dont let this thread die on me! LET ME READ IT ALL FFS!! FIRST REAL INTERESTING CRAP I READ ON /b/ besides TROLLING (that i sincerely love). PS: No one dare to SNIFF ritalin. I did and it almost fucked up my nose. i did it on RESEARCH system, rules and controls, and dude, NO FUCKING WAY IT IMPROVES ANYTHING THE USE OF METHILPHENIDATE. Its not that they dont want you to "be creative". Its just that any parenteral (not eating it, in plain language) of the drug IS USELESS AND LEADS TO ADDICTION AND JUST LEAVES YOU HIGH. Its pretty much like cocaine tho. PS: Verification LOL--> Anyjap visas ROFL

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Anonymous 06/04/11(Sat)07:26:27 No.332200664 File1307186787.jpg-(157 KB, 600x673, 1280528457061.jpg) >> Anonymous 06/04/11(Sat)07:28:07 No.332200866 >mfw this isn't 420chan >mfw I have no face 420chan.org. Get out of here drug heads Anonymous 06/04/11(Sat)07:29:29 No.332201013 Noradrenaline, adrenaline and epinephrine levels, as well as serotonine, have a strong relationship with Vitamine B3 availability. I used as much as 1g of B3 a day (CAREFUL: it gives you huge rash, so you have to get LOTS of info on how to use it, how to raise doses and so on, GOOOOOGLE ok?). Once you give your body enough B3 to produce serotonine noradrenaline and dopamine, ANY ADHD DRUG WORKS WAY BETTER, in my case, i needed 2 times less meds for the same effect. Anonymous 06/04/11(Sat)07:33:46 No.332201441 >>332200866 Since when you say what /b/ stands for? Wait, since when RANDOM stands for RANDOMdrugs? FU-CK YOU Anonymous 06/04/11(Sat)07:37:51 No.332201864 File1307187471.gif-(108 KB, 959x997, 1277665945141.gif)

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>>332200866 This is a discussion of neuroscience and biochem. And substances that affect the central nervous system. There's nothing wrong about learning knowledge in these things.