enchanted_elixir
𝕸𝖊𝖗𝖈𝖊𝖓𝖆𝖗𝖞 𝕮𝖔𝖗𝖕 • 𝟐𝟎𝟐𝟐🥉
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THE COMPLETE NOOTROPICS MASTERCLASS
VOLUME 3: THE LIST OF COMPOUNDS
PART 11 OF 11 | COMPOUND RANKINGS & STACKS
VOLUME 3: THE LIST OF COMPOUNDS
PART 11 OF 11 | COMPOUND RANKINGS & STACKS
Chapter 30 — My Assessment of Each Compound
This ranking is inevitably biased toward my own goals, physiology, experiences, and tolerance for risk. The commentary matters more than the letter beside each compound. The rankings have substance, but they are not the fourth law of thermodynamics, and a high ranking does not mean that a compound has strong human evidence or is safe for casual use.
I also distinguish between three things: what I have personally experienced, what other users commonly report, and what a mechanism merely predicts. Those are not interchangeable. An elegant mechanism can still produce nothing in a human, while an intense subjective effect can occur without improving cognition.
I will also say that unless explicitly stated, assume that I have not consumed the compound.
One final point: cellular energy does not normally feel like stimulation. When metabolic support works, it is closer to waking after a godly night of sleep and discovering that effort is cheap again. You do not necessarily feel pushed; you notice later that you remained sharp, recovered faster, and did not collapse when the demand became serious.
S — Fantastic
Bemitil: This is one of the most promising compounds in my eyes because its value should become clearest under genuine strain. The image is not forced stimulation; it is reaching the fifth difficult hour of thinking or training and realizing that your capacity is deteriorating much more slowly than expected. Its effects may build across several days, but the modern PK, sourcing, and long-term safety data remain much thinner than its reputation, and insomnia is a practical failure even if the day felt excellent.
ACD856: This is compelling because it appears to amplify the brain’s response to neurotrophins such as BDNF and NGF rather than indiscriminately forcing plasticity everywhere. In practical terms, the circuits you are actively using and reinforcing should receive the strongest learning signal. That makes it conceptually excellent for learning and deliberate habit change, but the human studies have established exposure and early safety—not that it makes healthy people smarter or creates a dependable subjective state.
TAK-653 / Osavampator: This is one of my favorite activity-dependent mechanisms. It amplifies AMPA signaling when glutamate has already arrived, so the ideal effect is that an already active line of thought becomes deeper, clearer, and easier to sustain rather than motivation being forced upon you. Reports from r/NooTopics include deeper thinking, improved mood, easier learning, and a higher perceived level of intelligence, but it accumulates for days and healthy-person cognitive enhancement has not been established.
Creatine Monohydrate: Creatine belongs here precisely because it is boring, inexpensive, and defensible. It enlarges the phosphocreatine reserve that helps cells regenerate ATP during repeated bursts of demand. You generally do not feel it arrive; you notice during prolonged thinking, sleep deprivation, repeated exercise, aging, or another energetic bottleneck that performance does not collapse as quickly and recovery between hard efforts is much faster. In my experience, a great compound.
A — Great
Intravenous NAD+: NAD+ is foundational to cellular energy transfer, but an infusion is not finished energy being poured directly into neurons. It guarantees delivery to the bloodstream while cells still decide how extracellular NAD+ and its breakdown products are processed and rebuilt. If it helps, it should feel like background energy has stopped fighting you rather than like stimulation; fast infusions can cause chest pressure, nausea, abdominal cramping, headache, and weakness, and that unpleasant reaction is not proof that the treatment is working harder.
SS-31 / Elamipretide: SS-31 targets cardiolipin in the inner mitochondrial membrane and is now a real, narrowly approved drug for Barth syndrome rather than merely an internet research peptide. The nootropic image is metabolic preservation: stressed mitochondria maintain their structure and output better, so fatigue arrives later. That mechanism is impressive, but rare-disease efficacy and dosing do not establish healthy-person cognitive enhancement.
Humanin: Humanin is a mitochondrial-derived survival signal that appears to help stressed cells resist injury through pathways distinct from SS-31. I rank the biology highly because preserving vulnerable cells could protect long-term capacity, not because Humanin has a reliable acute feeling. Controlled human phenomenology, dosing, chronic safety, and cancer-context data remain inadequate.
MOTS-c: MOTS-c is best viewed as an exercise-responsive mitochondrial signal, not literal exercise in a vial. If administered MOTS-c eventually proves useful, its benefit should appear under sustained demand as better metabolic flexibility and slower fatigue rather than as a stimulant rush. Native gray-market MOTS-c still lacks a validated administered-human dose, PK profile, and dependable subjective signature.
SLU-PP-332: SLU-PP-332 activates part of the endurance-exercise gene program through estrogen-related receptors, which makes it extremely interesting for mitochondrial and metabolic adaptation. The nuclear limitation is that it is still essentially a mouse research probe with poor practical drug properties and no established human dose or safety basis. I am ranking the concept and potential—not pretending that “cardio in a vial” has already been demonstrated in people.
Hypoxen: The attractive idea is functioning better when oxygen delivery becomes limiting, with fatigue appearing later during intense physical or cognitive demand. Reports describe lighter breathing and less exhaustion, but Hypoxen is a poorly characterized polymeric regional drug rather than a precise, validated mitochondrial electron shuttle. I see substantial potential, but its identity, PK, replication, and product consistency are unusually uncertain.
Meldonium: Meldonium changes mitochondrial fuel preference so that cells rely less on fatty-acid oxidation and can spend less oxygen for a given amount of ATP under ischemic or demanding conditions. It is usually not noticeable while sitting still; the difference should emerge six hours into difficult work or endurance exercise, when the normal energetic collapse is smaller and recovery into another work block is faster. The cardiovascular and physical evidence is much stronger than the healthy-cognition evidence, and glucose regulation, sleep, cardiovascular status, and anti-doping rules matter.
J147: J147 is a genuinely interesting neurotrophic-metabolic research compound linked preclinically to mitochondrial stress resistance and aging biology. The ideal effect would be quieter background energy and greater resilience rather than stimulation. There is still no controlled human cognitive profile, usable human PK, or established long-term safety, so this is an A-tier research direction in my assessment—not an A-tier evidence base.
BPN14770 / Zatolmilast: This PDE4D inhibitor prolongs cAMP–CREB signaling involved in memory formation and plasticity. Imagine completing a difficult trigonometry lesson and the cellular “save this” signal remaining active longer, giving the brain more opportunity to consolidate what was just learned. It has more human evidence than most experimental plasticity compounds, but that evidence comes mainly from impaired populations and does not prove healthy-person enhancement.
P-21 / P021: P-21 is an extremely experimental CNTF-derived peptide studied for neuronal survival, neurogenesis, and memory in animals. The useful picture is a hippocampus with better machinery for maintaining and building learning capacity, not an acute stimulant sensation. Nearly all of the impressive evidence ends in rodents, with no validated human dose, PK profile, or reproducible phenomenology.
Dihexa: Dihexa is fascinating because its proposed HGF/c-Met mechanism could push synaptic growth and connectivity extremely hard. I have heard @Clavicular describe an effect he interpreted as roughly a ten-point IQ increase, with faster learning and more sophisticated connections between ideas. That is a striking anecdote, not evidence of a predictable IQ gain or a known two-week human duration; human dose, PK, efficacy, and long-term growth-related safety remain unknown.
Cerebrolysin: Cerebrolysin has a substantial regional clinical history as an injectable porcine-brain peptide mixture, particularly in neurologic injury and disease. The strongest anecdotes come from impaired people who later realize that verbal access, emotional range, task persistence, or mental clarity has returned over days or weeks. That makes it more compelling for restoration after genuine dysfunction than for pushing an already optimized brain beyond baseline.
Cortexin: Cortexin occupies a similar restoration niche but should not simply inherit Cerebrolysin’s evidence or identity. It is a different, less precisely characterized animal-cortex peptide mixture with regional use and sparse modern pharmacology. Reports of reduced fog and easier word retrieval are interesting, but there is no single target, Tmax, half-life, or established healthy-user effect.
Cortagen: Cortagen is a defined four-amino-acid bioregulator, which makes it chemically cleaner than Cortexin, but not evidentially stronger. I like the idea of maintaining neuronal function and protecting irreplaceable neural tissue over time. The honest limitation is that trustworthy human exposure, timing, mechanism, and cognitive outcomes remain extremely thin.
Semax family: I have personally used a Semax product. In my experience it created greater motivation, a background sense of urgency, faster learning, and deeper retention for roughly four to five hours. This is the warrior version of the Semax–Selank comparison: it makes you want to move forward and gives active learning more force. Other people get nothing or develop anxiety, headache, fog, irritability, or insomnia, so my response is not universal.
The Three Main Semax Forms
- Original Semax — MEHFPGP: This is the actual regional medicine and the only version with the existing human clinical literature.
- N-acetyl Semax — Ac-MEHFPGP: The acetyl cap protects the front of the peptide from some enzymatic attack. That may increase stability, but it also changes the molecule; it is not automatically “Semax but better.”
- N-acetyl Semax amidate — Ac-MEHFPGP-NH₂: This caps both ends in an attempt to make the peptide harder to break down. It may last longer in theory, but there is no good comparative human study proving how much longer, stronger, or better it is.
The Three Main Selank Forms
- Original Selank — TKPRPGP: This is the form with the regional human anxiety evidence.
- N-acetyl Selank — Ac-TKPRPGP: The N-terminal acetyl cap is intended to slow breakdown from the front of the peptide, but no good human comparison proves that it works better.
- N-acetyl Selank amidate — Ac-TKPRPGP-NH₂: Both ends are capped to make enzymatic breakdown more difficult. It may be more stable, but its human duration, potency, safety, and superiority are unknown.
Modafinil and Armodafinil: These are the afinils with the strongest real human foundation. The characteristic effect is not a stimulant launch; it feels as if sleepiness has simply stopped being relevant, almost like waking ninety minutes after a good night of sleep and retaining that functional state for most of the day. They can preserve wakefulness and task availability, but they do not repay sleep debt and can produce robotic tunnel focus, headache, appetite loss, irritability, and insomnia.
Adrafinil, Flmodafinil, and Fladrafinil: I do not let these experimental or discontinued afinils inherit modafinil’s evidence merely because their names rhyme. Adrafinil adds slow and variable conversion plus liver concerns, while the fluorinated analogues have only fragmentary human metabolism data and gray-market sourcing problems. Their intended state may resemble delayed modafinil-like wakefulness, but the uncertainty is materially higher.
Bromantane: Bromantane’s appeal is calm background drive rather than an amphetamine shove. People often describe discovering two hours later that research, chores, exercise, and social action simply cost less effort, with less anxiety than a conventional stimulant. It may improve the intensity of an activity already begun more reliably than it creates the first decision to begin, and its long curve means sleep remains the practical test of whether it helped.
ASP-4345: I rank the D1 positive-allosteric-modulator concept highly because working memory is one of the fundamental pillars beneath fluid intelligence. The point is not a stimulant feeling. I would expect almost nothing at rest, then—when I actually invoke the DLPFC—a thought that stays on the mental whiteboard long enough to manipulate it, calculate with it, use it to contain an impulse, or return to it after distraction. This still requires adequate dopamine, metabolic support, and deliberate use of the circuit; ASP-4345 cannot generate the thought or the energy by itself. The clinical program did not establish meaningful cognitive benefit, so this remains an extremely attractive mechanistic simulation rather than a demonstrated healthy-user effect.
Tropisetron: Tropisetron is more than a nicotinic compound—it is a 5-HT3 antagonist with α7-nicotinic activity. The positive state is subtle, smooth filtering: irrelevant background noise loses pull and attention becomes easier to hold without stimulant urgency. Constipation, headache, fatigue, and dizziness are the reality check, and its healthy-person enhancement evidence remains weak.
Phenylpiracetam: I have tried phenylpiracetam, and for me it felt like becoming a laser aimed at a target. It combines racetam-like cognition with noticeable physical traction against fatigue, which makes it attractive for an exam, competition, cold exposure, or another exceptional demand. The spectacular first effect often fades quickly with repeated use, but the exact “once every one or two weeks” rule is an anecdotal strategy rather than a validated tolerance schedule.
Psychedelics — Psilocybin/Psilocin, LSD, N,N-DMT, 5-MeO-DMT, Mescaline, and Ibogaine/Noribogaine: I view these less as performance nootropics and more as tools for escaping a failing cognitive shell. They can temporarily destabilize the framework through which you interpret reality, yourself, and your inherited beliefs, making it easier to see that something treated like a law of physics was actually bullshit, emotionally inherited, or simply no longer useful. The benefit is returning with more possible ways to think; the danger is that psychedelics amplify the feeling that an idea is profound, not the probability that it is true. Every revelation must survive sober scrutiny, time, and results, and the risks of panic, mania, psychosis, cardiac harm in the case of ibogaine, dangerous behavior, and prolonged destabilization remain real.
Tabernanthalog: This has to remain separate from the hallucinogenic psychedelics. The extremely interesting part is that it may preserve the psychedelic deployment of attention without forcing somebody through the normal visual and reality-replacing trip. Arthur Juliani described ordinary vision becoming much more significant, spontaneous thought becoming quiet, and an almost supernatural patience for sitting with difficult thoughts and emotions for roughly nine hours. A larger collection of claimed users partially converges on equanimity, empathy, open-mindedness, introspection, and a “Zen” body high, which actually matches what this compound is supposed to do and makes the signal more meaningful than one random isolated claim. Higher-exposure reports also describe nausea, dizziness, bed-lock, gastrointestinal destruction, and an unmistakably altered psychedelic or dissociative state, so “non-hallucinogenic” does not mean non-psychoactive or safe. The products and exposures were not clinically verified, but these reports are still useful preliminary human evidence rather than noise. Detailed phenomenological report · Collection of additional reports
GB-115 / Ranquilon: The attractive report is that the physical alarm component of anxiety becomes much quieter while cognition remains intact or even mildly sharpened. That could mean remaining level-headed in a situation that normally consumes working memory with threat. “Entirely immune to anxiety and cortisol spikes” is too absolute; GB-115 has small human PK and clinical data, but the dramatic forum phenomenology is sparse and under-replicated.
Aticaprant: Aticaprant antagonizes kappa-opioid receptors, a system associated with stress-linked dysphoria and reduced reward pursuit. The useful state would not be euphoria; it would be rejection or chronic dysphoria losing its power to make every future action seem pointless, allowing somebody to bounce back and pursue ordinary rewards again. The concept is excellent, but the clinical program has disappointed and there is no dependable healthy-user phenomenology.
Orexin A: Orexin biology may be the cleanest possible wakefulness target: instead of feeling stimulated, you simply remain stably awake, as if a nap had been compressed into a nasal spray. The native peptide is nevertheless a terrible practical drug because it is fragile and brain delivery is unreliable; anecdotes range from several hours of pristine wakefulness to absolutely nothing, sometimes with rapid tolerance. I rank the orexin system highly, but I rank gray-market native Orexin A much less confidently than a real brain-penetrant OX2R agonist.
B — Good
Sarcosine: Sarcosine inhibits GlyT1, leaving more glycine available at the NMDA receptor’s co-agonist site. Responders describe less internal blockage, easier social presence, and ordinary tasks becoming possible without a stimulant forcing them forward. Most serious evidence is in schizophrenia-spectrum and impaired populations, so I view it as a restoration compound rather than a reliable intelligence enhancer for an already healthy person.
5-Amino-1MQ: This experimental NNMT inhibitor is interesting because NNMT participates in nicotinamide and methyl-group metabolism, making it a plausible metabolic target in aging and obesity. The current Chapter 18 profile correctly limits the promise: there is essentially no human dosing, PK, cognition, or long-term safety science. I rank the metabolic idea, not the gray-market claims of sustained cellular energy or effortless fat loss.
Vinpocetine: I have personally taken vinpocetine and experienced a clearer, less congested head consistent with its short-acting neurovascular profile. I cannot literally feel cerebral blood flow, and more flow is not automatically more intelligence; the payoff depends on whether vascular delivery was actually a bottleneck and what the blood is carrying. Headache, dizziness, low blood pressure, pregnancy risk, and weak healthy-cognition evidence keep it in B rather than A.
Low-Dose Tadalafil / Cialis: Tadalafil can improve systemic vascular signaling for a much longer period than vinpocetine, but it is not brain-specific. If vascular dysfunction is limiting cognition, some people may feel more present or less foggy; if it is not, the most memorable effect may be a day-long headache, congestion, reflux, or dizziness. This is a prescription vascular drug with possible cognitive consequences, not a cerebral-flow supplement.
NSI-189: NSI-189 is a highly variable investigational neurogenic antidepressant candidate rather than a simple hippocampus-regeneration drug. Positive reports describe richer emotion, curiosity, verbal access, motivation, and memory returning over days; negative reports include head pressure, fatigue, insomnia, visual changes, intrusive thoughts, mania, or psychosis. Most clinical work used the phosphate salt, so gray-market freebase reports do not automatically inherit that PK or safety record.
PRL-8-53: The famous effect is information fading less after it has been learned, sometimes appearing as surprisingly strong recall the following day rather than as an acute “smart” feeling. That reputation rests mainly on one small 1978 human study plus anecdotes. Human PK, replication, chronic safety, and a modern product standard are missing, so reports of problems after several weeks deserve caution without becoming a precise validated cutoff.
Paraxanthine: Paraxanthine is caffeine’s principal active metabolite taken directly. For some people it feels like caffeine’s useful middle—wakefulness and task availability with less tremor, stomach irritation, or anxious peripheral noise. It is not automatically stronger or cleaner, and for others it feels like ordinary caffeine, weak caffeine, delayed sleep disruption, or nothing.
Methylphenidate: In a well-matched ADHD patient, methylphenidate may feel less like stimulation and more like twenty televisions in the same room being reduced to one. It strengthens the grip on a selected signal, which can make ordinary execution possible but can also lock attention onto the wrong task. It is often calmer and less propulsive than amphetamine, while still carrying appetite, sleep, cardiovascular, dependence, and rebound costs.
Adderall / Mixed Amphetamine Salts: Adderall contributes more propulsion than methylphenidate: boring work can feel urgent, fatigue recedes, and continuing requires much less willpower. The nuclear problem is that the propulsion has no steering wheel, so gaming, arguing, cleaning one irrelevant corner, or researching nonsense can become the sacred mission. In ADHD this can be transformative; outside a legitimate indication it can purchase apparent productivity with sleep loss, appetite suppression, cardiovascular strain, tolerance, dependence, and confidence that outruns accuracy.
Vyvanse / Lisdexamfetamine: Vyvanse is gradually converted into dextroamphetamine, so the rise and fall often feel smoother and less abrupt than immediate-release amphetamine. A responder may simply notice that messages were answered and one document remained open without hours of negotiation. Smooth does not mean weak or harmless: appetite can disappear all day, emotion can flatten, insomnia can extend late into the night, and smooth hyperfocus can still be hyperfocus on the wrong thing.
Selegiline / Deprenyl: At conventional low oral exposure, selegiline primarily inhibits MAO-B, allowing dopamine and phenethylamine signaling to last longer; it does not simply preserve dopamine, norepinephrine, and serotonin equally at every dose and route. Some users report subtle wakefulness, libido, curiosity, and less friction beginning tasks, while others feel nothing or develop insomnia, irritability, hypomania, or paranoia. The parent drug clears quickly but irreversible enzyme inhibition lasts for days, making interactions and route differences central.
AF710B / ANAVEX3-71: I have personally taken AF710B and noticed that information entered and remained more effectively, colors appeared sharper, and working memory improved mildly. The useful effect was clearer in retrospect than as an acute “hit.” It combines M1 muscarinic and sigma-1 signaling, has real early human PK, and may interact strongly with other cholinergics; more choline is not automatically better if cholinergic side effects appear.
Aniracetam: This is the socially loose racetam. Positive reports describe words becoming more available, music becoming richer, conversation becoming less overanalyzed, and background social anxiety turning down without intoxication. It is fat-soluble and the parent is short-lived while metabolites matter substantially; sedation, bodily anxiety, irritability, headache, and nonresponse are all common enough to keep expectations modest.
Oxiracetam: This is the clean, technical-work racetam in my eyes. Mathematics, coding, accounting, or lecture material may become more linear—fewer useless branches, cleaner recall, and mild activation without stimulant propulsion. It does not create motivation, and some people become sleepy, irritable, foggy, or almost slightly drunk.
Coluracetam: Coluracetam is famous for the “HDR vision” report: colors become more saturated, music becomes more absorbing, mood brightens, and focus feels calm. Its proposed high-affinity choline-uptake mechanism is more specific than simply adding acetylcholine, but human evidence and public PK remain extremely thin. Headache, nausea, dysphoria, and persistent visual changes belong in the risk column, and sharper colors are not proof of optic-nerve repair or cognitive improvement.
Noopept: I have taken Noopept and experienced faster learning and operation, sharper senses, and useful mental endurance. Stacking it with the Semax product I used was especially strong for me: I read a copywriting book front to back in one sitting and retained far more than I ordinarily would. Other people experience cold task focus, while some become irritable, emotionally numb, forgetful, foggy, or anxious, and human PK remains incomplete.
L-Theanine: Theanine is inexpensive and useful primarily because it subtracts noise. It can smooth caffeine, loosen physical tension, and silence some background thinking without creating energy of its own. If somebody is already flat, sleepy, hypotensive, or unmotivated, the same reduction in arousal can reduce function rather than improve it.
Ashwagandha: Ashwagandha requires sustained use and makes the most sense when excessive stress is consuming cognitive bandwidth. The positive result is that an exam, argument, or deadline still matters, but the body does not accelerate as far and rumination does not loop as long. The failure mode is mistaking apathy, lower libido, reduced urgency, or emotional flattening for resilience.
Rhodiola rosea: In my experience, Rhodiola works best on an empty stomach and gives a mild adrenergic background lift that makes fatigue less adhesive. It is most useful when stress-linked fatigue is the actual bottleneck and may become more apparent over repeated use. If somebody is already anxious, manic-prone, or underslept, it can turn exhaustion into wired exhaustion.
Kanna / Sceletium tortuosum: Kanna can create warmer mood, greater sociability, tactile interest, and less interpersonal friction, which makes it interesting for social contexts. The product matters enormously: weak standardized oral extracts and potent high-mesembrine products are functionally different exposures. Some users get a pleasant social lift; others get nausea, pressure, jaw tension, dizziness, or serotonergic jitters that make them worse at reading the room.
Low-Dose Lithium Orotate: The potential value is reduced emotional whiplash: more pause between feeling something and reacting, with rejection or irritation becoming less capable of detonating the whole day. Evidence for supplemental lithium orotate and longevity is not strong enough to present as settled. The unwanted version is a spaced-out, flattened state with lower libido, thirst, tremor, acne, fatigue, or reduced warmth.
Mitragynine / Green Vein Kratom: At the right exposure, kratom can feel like warm social armor: calm, pleasure, pain relief, and a sense that life is good while some energy remains. Too much becomes sedation, nausea, sweating, itching, sexual dysfunction, or poor social perception. Its immediate usefulness is precisely what makes dependence dangerous; repeated use can make baseline social life feel anxious, empty, and physically painful until another dose is taken.
Emoxypine Succinate / Mexidol: Emoxypine is most interesting when oxidative and stress-related noise is making the brain feel foggy or overreactive. Positive reports describe physical tension softening while the mind remains relatively clear, rather than a dramatic stimulant effect. Regional evidence, formulation differences, sleepiness, fog, and product-quality uncertainty prevent confident healthy-user claims.
Indolepropionamide (IPAM): Indolepropionamide (IPAM) is a fascinating mitochondrial hypothesis with almost no human map. Sparse reports range from deep background energy and improved endurance to lethargy, odd sensations, or nothing. There is no validated human dose, PK, safety profile, or proof that a subjective energy change reflects the proposed mitochondrial mechanism.
Glutathione: Glutathione is a central redox buffer, not an automatic nootropic. A depleted or highly stressed person may report cleaner energy, a slightly larger fatigue envelope, or less fog after an effective formulation, while a healthy person may notice nothing. Oral formulations, liposomal products, and injections create different exposures and risks, and the first question should be what is overwhelming the redox system rather than how invasive the delivery can be.
Pregnenolone: I have taken pregnenolone and experienced brighter colors, a somewhat more plastic feeling, and slight cerebral pressure or vasoconstrictive sensation. It is a lipophilic neurosteroid and precursor that can feed progesterone, DHEA, allopregnanolone, pregnenolone sulfate, and sex-hormone pathways, so the response is not predictable. Clarity and emotional vividness are possible, but so are sedation, insomnia, irritability, acne, libido changes, and hormonal instability.
Sunifiram and Unifiram: These are racetam-adjacent excitatory plasticity compounds, not ordinary racetams. Positive reports describe bright, fast recall, intensified perception and music, and more room to manipulate ideas without a stimulant body load. The evidence problem is catastrophic: neither has a proper human PK, dose-finding, or long-term safety program, and amplifying learning signals can strengthen useful learning, anxiety loops, or overstimulation with equal indifference.
Uridine Monophosphate, DHA, and Choline: This is a slow structural stack rather than something that should “hit.” Uridine supplies nucleotide material, DHA supplies a major neuronal-membrane fat, and choline supplies phospholipid and acetylcholine material. Together they provide building materials for membranes and synapses, but materials do not command the brain to build useful circuits without learning and activity, and the loose three-part stack does not inherit every result from more complete medical-food formulas.
Growth Hormone, GHRH Analogues, and the IGF-1 Axis: This belongs in B tier as a restoration and recovery axis, not as a casual intelligence shortcut. Older, deficient, or impaired people may notice deeper sleep, better recovery, reduced fog, or greater endurance, and controlled GHRH data provide a limited cognition signal in older adults. The signal is not brain-specific: edema, carpal-tunnel-like symptoms, worsened sleep apnea, glucose intolerance, insulin resistance, and unwanted tissue growth are real tradeoffs, while direct IGF-1 and unapproved IGF-1 LR3 are much blunter and riskier than upstream GHRH approaches.
C — Meh
Pyrroloquinoline Quinone / PQQ: PQQ is a redox-active mitochondrial signal, not instant fuel. It is often described as influencing pathways including PGC-1α, but claims that one capsule simply commands neurons to manufacture mitochondria are too clean. The realistic outcome is either nothing or a slow reduction in background fatigue, with modest human evidence and possible insomnia or overstimulation.
R-1,3-Butanediol: I have tried this through Ketone-IQ and experienced smooth alertness without jitters, greater sensory intensity, and easier learning when metabolically healthy. It is converted in the liver into R-BHB and can provide temporary alternative fuel, but it also uses alcohol-related metabolic pathways and may produce nausea, headache, or an impairing alcohol-like state. “Ketohol” should not be assumed compatible with driving or precision work.
Caffeine: Caffeine is effective at blocking sleep-pressure signaling and making work feel more urgent, but it does not create energy or repay recovery. For me, the adrenergic, jittery, anxious, and vasoconstrictive texture often nukes the benefit unless I pair it with theanine. The useful dose clears fog; the excessive dose makes the body feel as if an emergency has begun.
KW-6356 / Sipagladenant: This feels conceptually like an extremely persistent, selective A2A brake release rather than merely “paraxanthine on steroids.” Reports describe effortless task initiation and long-lived focus, but the same duration can mean appetite loss, tunnel vision, and being unable to sleep after the productive feeling has ended. It is an abandoned experimental drug with no validated healthy-user dose, and one poor decision may disrupt several days.
L-Tyrosine: Tyrosine is precursor insurance, not biochemical amphetamine. It is most useful when cold, acute stress, sleep loss, or sustained demand makes catecholamine precursor availability more limiting; then working memory and cognitive control may fail less abruptly. In a well-fed, rested person without a precursor bottleneck, feeling nothing is the ordinary outcome.
Mucuna pruriens: In my experience, Mucuna was more useful for physical performance and perseverance than for motivation, and I previously explored it for shortening the refractory period. Its main active ingredient is real L-DOPA, which makes it pharmacologically serious rather than gently “natural.” Product-to-product L-DOPA exposure is extremely variable, and nausea, dizziness, insomnia, abnormal movement, mania, hallucinations, and compulsive behavior are possible.
9-Methyl-β-Carboline / 9-Me-BC: In my experience, this resembled background MAO inhibition: dopamine-related drive felt more persistent, but it could not be mobilized into useful behavior. The preclinical dopaminergic-restoration story is fascinating, while controlled human efficacy and usable human PK are nonexistent. Photosensitivity and photochemical concerns appear in the experimental and anecdotal record, and the unknown interaction footprint makes casual stacking difficult to justify.
IDRA-21: IDRA-21 is a much messier and less developed version of the AMPA-modulation idea that makes TAK-653 attractive. Some users describe information sticking or working memory feeling wider, while others report headache, fog, insomnia, mood deterioration, or nothing. It has memorable animal and primate data but no usable human dose, Tmax, half-life, clearance, or safety program.
Choline Bitartrate: This is an inexpensive way to raise plasma choline, not a reliable nootropic on its own. It can correct low intake or occasionally remove a cholinergic-stack headache, but many people feel nothing and excess can cause pressure headache, nausea, lethargy, low mood, diarrhea, or fishy odor.
Alpha-GPC: Alpha-GPC is a concentrated, water-soluble choline donor that can make thought-to-speech translation, visual crispness, or mind-muscle connection feel cleaner in a responder. The characteristic bad response is a headache combined with anxious bodily activation or flat, heavy “cholinergic depression.” It is useful when it solves a demonstrated bottleneck, not as mandatory decoration on every racetam stack.
Citicoline / CDP-Choline: Citicoline supplies choline plus cytidine-derived material that enters the uridine pathway, so it is more than a simple acetylcholine precursor. Responders describe smoother background wakefulness, cleaner reading, and less impulsive task-switching; others become anxious, headachy, flat, lethargic, or unable to sleep. It has real human pharmacology but uncertain value for an already healthy young reader.
Phosphatidylcholine: Phosphatidylcholine is the slow, food-like choline option and a membrane-building nutrient rather than an acute focus switch. It may be useful for nutritional support or tolerability, but a lecithin label does not reveal how much phosphatidylcholine or choline is actually present. Most people should expect subtle effects or none.
Galantamine: Galantamine is more convincing as a lucid-dream inducer than as a healthy daytime nootropic. It can make dreams intensely vivid and increase the chance of recognizing that one is dreaming, but it can also turn the night into nausea, sweating, muscle tension, slow pulse, anxiety, and insomnia. It is a prescription-level cholinesterase inhibitor, not merely a dream supplement.
Huperzine A: Huperzine A also prevents acetylcholine breakdown, but it is potent, long acting, and measured in micrograms. I noticed some lucid-dream utility from Huperzine A and choline bitartrate without an impressive daytime cognitive effect. Its long duration makes excessive cholinergic effects—nausea, cramping, sweating, twitching, headache, slow pulse, and ruined sleep—difficult to outwait.
Bacopa monnieri: Bacopa is a slow memory compound. The benefit may appear eight to twelve weeks later when names, vocabulary, or studied material are simply easier to retrieve, not as an acute sensation. The filing cabinet can improve while the office closes early: fatigue, flattened motivation, fog, and vivid dreams can erase the real-world value if they reduce how much you study.
Oroxylin A: The proposed combination of dopamine-transporter and GABA-A effects sounds like greater focus with fewer brakes, but almost all of the strong evidence is preclinical. Pure Oroxylin A and a Sabroxy-style botanical extract are not the same exposure. Reports range from mild stimulation to anxiety, headache, dysphoria, insomnia, and feeling physically awful, so removing inhibition is not automatically cognition.
Ginkgo biloba: A properly standardized Ginkgo extract can make a thin layer of haze disappear for some people, particularly when vascular or age-related impairment contributes to the bottleneck. Most healthy people notice little, and generic leaf powder or tea cannot inherit the evidence for quantified EGb 761-type extracts. Headache is not proof that more blood reached the brain, and subjective clarity is not proof that memory improved.
Piracetam: Piracetam is the original and probably the most subtle racetam. If it works, cognitive friction decreases: fewer word-search pauses, easier associations, and long reading sessions feeling less abrasive. Many healthy users feel absolutely nothing, while others get headache, fog, irritability, or a sharper feeling without better work.
Pramiracetam: Pramiracetam is narrow, emotionally dry focus. Responders describe blinders coming down so one textbook, spreadsheet, or problem occupies the foreground and everything else loses priority. That helps only when the correct task was chosen; it can also make somebody rigid, antisocial, or joyless, and it supplies neither motivation nor judgment.
Fasoracetam: Fasoracetam’s attractive profile is calm focus: the internal argument about beginning work becomes quieter, anxiety recedes, and speech flows without a classic stimulant feeling. Other users report sedation, fog, restlessness, sexual side effects, or nothing. Its internet reputation as a phenibut or baclofen “tolerance reset” is not established in humans and should not become a home-withdrawal protocol.
Nefiracetam: Positive reports describe cognition becoming usable again rather than aggressively accelerated: fog lifts, anxiety quiets, recall improves, and mood remains stable. That smoothness sits beside unresolved animal renal and testicular toxicology and a weak healthy-human enhancement record. Feeling smooth does not make chronic exposure safe.
Kava / Piper methysticum: Kava can create loose, warm social calm, a numb mouth, and less physical tension without reproducing alcohol’s exact state. It can still impair coordination, reaction, judgment, and motivation, especially as the dose rises. Traditional noble-root water preparations and concentrated extracts are not interchangeable, and relaxation is not automatically better social performance.
Panax ginseng: Panax can provide calm readiness and a smaller voltage drop across a long day, but the response depends heavily on extract, processing, and microbiome. It is not accurate to say that every ginseng product simply raises cellular ATP over time. The cognitive effects are usually modest and the opposite response can be insomnia, palpitations, irritability, or fatigue.
Schisandra chinensis: Schisandra may make a long day feel less frayed, with mild calm energy rather than stimulation. Healthy cognitive evidence is weak, formulations vary substantially, and its interaction footprint is serious enough to matter. It is a poor casual experiment for somebody taking interaction-sensitive medication.
Eleuthero / Eleutherococcus senticosus: Eleuthero is more coherent as a physical-fatigue and work-capacity aid than as a direct memory compound. If it works, you discover the difference by finishing the workout or long day with more reserve rather than by feeling euphoric. It is not Panax ginseng, and vague “adaptation” without improved output is not enough.
Lion’s Mane: In my experience, properly formulated Lion’s Mane can improve learning and memory over time rather than producing an acute hit. Product identity is the nuclear issue: fruiting-body and mycelial products contain different chemistry, and generic powder cannot inherit every extract study. My preferred general-purpose form is a tested fruiting-body dual extract using both hot-water and alcohol extraction; nighttime use may suit someone who becomes sleepy or notices vivid dreams, but it should be moved earlier or stopped if sleep fragments.
Nicotinamide Riboside / NR: NR is a measurable, water-soluble NAD precursor with real human metabolism data. Most healthy young people should expect no acute feeling, while older or metabolically strained responders may notice calmer background energy over days or weeks. Raising a NAD-related biomarker is not itself proof of better cognition.
Nicotinamide Mononucleotide / NMN: NMN is another NAD precursor, one biochemical step closer on paper but not automatically better in a person. Responders describe subtle energy or easier exercise; others feel nothing or develop activation and insomnia. Product quality, baseline status, and objective outcomes matter more than the “one step closer” marketing line.
D — Underwhelming
URB597: URB597 is an elegant FAAH-inhibition idea because it lets locally produced anandamide last longer instead of directly flooding every cannabinoid receptor. The most vivid two-day report described catastrophic overcorrection: anxiety disappeared so completely that overdue coursework stopped feeling urgent, the person remained in bed, thinking became hazier, and even strong coffee or prescribed Adderall XR subjectively failed to restore normal drive. Everything felt resolved while nothing had actually been resolved. Other old reports range from contentment and quieter bad thoughts to stimulation, sedation, next-morning laziness, or anxiety, with doubtful product identity throughout. That possible transformation of resilience into apathy is why I keep it in D despite the brilliant mechanism.
Bupropion: I have been prescribed bupropion. In my experience it removed the defeated, inert form of depression, which can be tremendously valuable when depression is the bottleneck, but it did not function as a general cognitive enhancer. Other people experience a motivating honeymoon, anxiety, insomnia, irritability, tinnitus, emotional flattening, or worse cognition, and seizure risk makes casual stimulant-style use inappropriate.
Saffron: Saffron has a more credible human mood literature than my personal response would suggest, but it did nothing noticeable for me. Its expected benefit is gradual reduction in negative bias or rumination over weeks, not an acute nootropic hit. Personal nonresponse keeps it in D for my ranking without proving that standardized extracts are universally ineffective.
F — Ineffective
Phenibut / β-Phenyl-GABA: I tried phenibut during a new semester for anxiety and experienced little beyond mildly reduced social inhibition. Some responders describe dramatic social ease, but delayed onset, redosing, tolerance, dependence, rebound anxiety, insomnia, hallucinations, and seizure risk make that benefit a terrible bargain. For my goals, GB-115 plus L-theanine conceptually mogs a compound that either does little or risks replacing anxiety with disinhibition and dependence.
Z — Dislike
Nicotine: Nicotine can sharpen attention rapidly, especially through regulated gum or lozenges, but that effectiveness is exactly why it is a poor bargain for a nicotine-naïve person. With repetition, the “focus” increasingly becomes relief from the fog and craving created by the previous dose. Tropisetron offers a non-reinforcing nicotinic-adjacent concept without deliberately creating a nicotine dependence loop, although it is not a direct substitute.
Benzodiazepines, Barbiturates, Alcohol / Ethanol, Baclofen, Gabapentin, and Pregabalin: These compounds can be valuable medicines when panic, seizures, spasticity, neuropathic pain, or pathological arousal is the actual problem. As general performance enhancers, however, they usually purchase calm by subtracting alertness, memory, reaction speed, judgment, or motor control, with dependence risk for several members of the group. Removing a genuine pathological bottleneck can indirectly improve function; sedating a healthy nervous system is not the same thing as improving cognition.
Chapter 31 — Stacks
These are stacks I would consider if I had unlimited funds, did not mind spending ten minutes taking multiple compounds, and had already established that my health was solid. They are conceptual maps, not instructions to take everything simultaneously.
Anti-Anxiety/Anti-Stress/Mood Stack
- GB-115
- Aticaprant
- L-theanine
- Mitragynine/Green Vein Kratom
- Selank family
- Low-Dose Lithium
- Kanna
Peak Performance Stack
- Bemitil
- Modafinil
- Bromantane
- Semax family
- Creatine
- Tropisetron
- Phenylpiracetam + Alpha-GPC
- Hypoxen
- Meldonium
- TAK-653 (or Noopept)
- Cortagen
- Pinealon
- J-147
- SLU-PP-332/MOTS-C
- ASP-4345
- Vinpocetine
- Emoxypine Succinate
Peak Learning Stack
- ACD856
- BPN14770
- Semax family
- Dihexa
- Aniracetam/Oxiracetam/AF710B + Alpha-GPC
- Noopept
- PRL-8-53
- Vinpocetine
- Pinealon
Cognitive Transformation Stack
- Tabernanthalog
- Low-Dose Psychedelics
- ACD-856
- Selank family
- BPN14770
Cognitive Regeneration Stack
- Cerebrolysin/Cortexin
- NSI-189
- Vinpocetine
@Volpa #Volpamogs
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