21 replies to this topic

[Grandmaster]

Hello

Im looking for nootropic that  would significantly improve logical thinking so it would make easier understanding mathematics and other logical thinking based things. I have used noopept for a month and it had improved logical thinking abilty but also caused short term memory loss so it wasnt so great experience.

 

 

 

[Busyboy]

Bump

[Blackkzeus]

Semac
Semax*

[nootist]

Were I facing a software release day, or a chess tournament, I would be reaching for the pramiracetam.

[Busyboy]

Any "natural" supplements for logic enhancing? Like Huoerzine, Tyrosine or Bacopa?

[Grandmaster]

Any "natural" supplements for logic enhancing? Like Huoerzine, Tyrosine or Bacopa?

 

I have used huperzine in the 2014 for near 2 months and it gave me little memory boost as i have memorized any dream when taken 100mcg before sleeping. I dont think that it improves logical thinking

[gamesguru]

sorry, just regurgitating an incomplete list, verbatim from an old post:

Effects of alcohol aqueous extract from Rhodiola rosea L. roots on learning and memory
Using the maze-method with negative (punitive) reinforcement, it has been found that  Rhodiola extract in a single dose of 0.10 ml per rat essentially improves learning and retention after 24 hours . Significant improvement of the long-term memory is also established in memory tests after 10-day treatment with the same dose of the extract. In the other two doses tested (0.02 and 1.0 ml per rat) the extract has no substantial effect on learning and memory. In a dose of 0.10 ml per rat the Rhodiola extract had a favou rable effect on the training process using the "staircase" method with positive (food) reinforcement as well. With the other methods used (active avoidance method with negative reinforcement "shuttle-box" and passive avoidance methods "step down" and "step through") Rhodiola extract in the dose used (0.10 ml per rat) had no substantial effect on learning and memory

 

Effect of bacoside extract from Bacopa monniera on physical fatigue induced by forced swimming.

The antifatigue effect of bacoside extract (BME) from Bacopa monniera (L.) Wettst. was investigated. Rats were subjected to weight-loaded forced swim test (WFST) every alternate day for 3 weeks. The BME at a dosage of 10 mg/kg body weight was administered orally to rats for 2 weeks in order to evaluate the following biomarkers of physical fatigue: swimming time, change in body weight, lipid peroxidation, lactic acid (LA), glycogen, antioxidant enzyme activities such as superoxide dismutase (SOD) and catalase (CAT) and blood parameters, namely blood urea nitrogen (BUN) and creatine kinase (CK). The exhaustive swimming time was increased by 3-fold in the BME supplemented group compared with that of the control group on day 13. The BME treatment lowered malondialdehyde (MDA) levels in brain, liver and muscle tissues by 11.2%, 16.2% and 37.7%, respectively, compared with the control exercised group (p < 0.05). The BME also reduced the LA, serum BUN and CK activities significantly compared with that of the control. Administration of BME significantly protected the depletion of SOD and CAT activities. The HSP-70 expression studies by western blot also confirmed the antifatigue property of BME. The present study thus indicates that BME ameliorates the various impairments associated with physical fatigue.

 

An open-label study to elucidate the effects of standardized Bacopa monnieri extract in the management of symptoms of attention-deficit hyperactivity disorder in children.

SBME significantly reduced the subtests scores of ADHD symptoms, except for social problems. The symptom scores for restlessness were reduced in 93% of children, whereas improvement in self-control was observed in 89% of the children. The attention-deficit symptoms were reduced in 85% of children. Similarly, symptom scores for learning problems, impulsivity, and psychiatric problems were reduced for 78%, 67%, and 52% of children, respectively. It was observed that 74% of the children exhibited up to a 20% reduction, while 26% of children showed between a 21% and a 50% reduction in the total subtests scores.  Standardized extract of B monnieri was found to be effective in alleviating the symptoms of ADHD and was well-tolerated by the children.

 

Effects of 12-Week Bacopa monnieri Consumption on Attention, Cognitive Processing, Working Memory, and Functions of Both Cholinergic and Monoaminergic Systems in Healthy Elderly Volunteers
At present, the scientific evidence concerning the effect of Bacopa monnieri on brain activity together with working memory is less available. Therefore, we aimed to determine the effect of B. monnieri on attention, cognitive processing, working memory, and cholinergic and monoaminergic functions in healthy elderly. A randomized double-blind placebo-controlled design was utilized. Sixty healthy elderly subjects (mean age 62.62 years; SD 6.46), consisting of 23 males and 37 females, received either a standardized extract of B. monnieri (300 and 600 mg) or placebo once daily for 12 weeks. The cholinergic and monoaminergic systems functions were determined using AChE and MAO activities. Working memory was assessed using percent accuracy and reaction time of various memory tests as indices, whereas attention and cognitive processing were assessed using latencies and amplitude of N100 and P300 components of event-related potential. All assessments were performed before treatment, every four weeks throughout study period, and at four weeks after the cessation of intervention. B. monnieri-treated group showed improved working memory together with a decrease in both N100 and P300 latencies. The suppression of plasma AChE activity was also observed. These results suggest that B. monnieri can improve attention, cognitive processing, and working memory partly via the suppression of AChE activity.

 

Learning and memory-enhancing effect of Bacopa monniera in neonatal rats.
The aim of this study was to evaluate the learning and memory-enhancing effect of Bacopa monniera in neonatal rats.
Learning is an acquisition and storage of information as a consequence of experience. Memory is a relatively permanent storage form of the learned information. In the process of 'learning', activation of neurons occurs in specific areas or specific memory systems of the brain concerned with the processing of the specific modality of sensory information. Rasayana plants are said to prevent ageing, re-establish youth, strengthen life, brain power and prevent diseases. Bacopa monniera (BM) is shown to be very useful in improving learning and memory.
In the present study neonatal rat pups (10 days old) were given different doses of BM extract orally for different periods of time. These rats were then subjected to spatial learning (T- Maze) and passive avoidance tests along with the age matched normal and gum acacia control rats. The data were compared with those of control rats.
The results showed improvement in spatial learning performance and enhanced memory retention in neonatal rats treated with extract of BM.

We conclude that treatment with BM extract during growth spurt period of neonatal rats enhances learning and memory (Tab. 3, Fig. 3, Ref. 45). Full Text in free PDF www.bmj.sk.

Effect of Bacopa monniera Linn. (brahmi) extract on learning and memory in rats: A behavioral study
Extracts of Bacopa monniera (Brahmi, BM), a traditional ayurvedic medicine, have been reported to have memory-enhancing effects in animals. However, there are no studies in which different dosages or chronic use have been explored. The current study examined the effects of standardized extract of BM on behavioral changes of Wistar rats when administered the extract for various durations and in varying doses. We divided the animals into 2-, 4-, and 6-week treatment groups. Rats in each of these groups were divided into 20 mg/kg, 40 mg/kg, and 80 mg/kg dose groups (n=8 for each dose). After the treatment period, the rats, along with age-matched normal and gum acacia control rats, were subjected to spatial learning (T-maze) and passive avoidance tests. The data were compared with those of age-matched control rats. The study was conducted at the Melaka Manipal Medical College, Manipal University, Manipal, Karnataka, India. The results showed improvement in spatial learning performance and enhanced memory retention in rats treated with BM extract. These results clearly indicate that oral administration of BM extract improved learning and memory in rats.

 

Panax ginseng (G115) improves aspects of working memory performance and subjective ratings of calmness in healthy young adults

Extract of Ginkgo biloba leaves reverses yohimbine-induced spatial working memory deficit in rats

Green tea extract enhances parieto-frontal connectivity during working memory processing

Plant-Derived Flavanol (−)Epicatechin Enhances Angiogenesis and Retention of Spatial Memory in Mice

Sonchus asper: brain antioxidant markers, cognitive performance and acetylcholinesterase activity of rats

Effect of a polyphenol-rich wild blueberry extract on cognitive performance of mice, brain antioxidant markers and acetylcholinesterase activity

Edited by gamesguru, 22 September 2015 - 08:37 PM.

[Blackkzeus]

What truly enhances my logical thinking the most to where I feel like I understand almost anything is, Methyl Drive 2.0. It's a thermogennic, but there's something in there that really boosts cognition.

[Area-1255]

Any "natural" supplements for logic enhancing? Like Huoerzine, Tyrosine or Bacopa?

HuperZine A is also an NMDA antagonist; which may not be the best idea for logic/common sense. Seeing as how glutamate is necessary for logic and communication and Autistics are seen with deficits in glutamatergic transmission.

 

 

Neuroscience. 2001;105(3):663-9.

Huperzine A, a nootropic alkaloid, inhibits N-methyl-D-aspartate-induced current in rat dissociated hippocampal neurons.

Zhang JM1, Hu GY.

Author information

 

Abstract

Huperzine A, a nootropic alkaloid isolated from a Chinese herb, has been proposed as one of the most promising agents to treat Alzheimer's disease. Recently, the agent was found to inhibit the N-methyl-D-aspartate (NMDA) receptors in rat cerebral cortex in addition to causing an inhibitory effect on acetylcholinesterase. In the present study, the mechanisms underlying NMDA receptor inhibition were investigated using whole-cell voltage-clamp recording in CA1 pyramidal neurons acutely dissociated from rat hippocampus. Huperzine A reversibly inhibited the NMDA-induced current (IC(50)=126 microM, Hill coefficient=0.92), whereas it had no effect on the current induced by alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate or kainate. The effect was non-competitive, and showed neither 'voltage-dependency', nor 'use-dependency'. The IC(50) values of huperzine A were neither altered by changing the concentrations of glycine (2-0.2 microM) and pH (7.4-6.7) in the external solution, nor by addition of Zn(2+) (5 microM) and dithiothreitol (5 mM) to the external solution. However, addition of spermine (200 microM) to the external solution caused a parallel shift to the right of the huperzine A concentration-response curve. From these we suggest that huperzine A acts as a non-competitive antagonist of the NMDA receptors, via a competitive interaction with one of the polyamine binding sites. The potential relevance of NMDA receptor antagonist activity of huperzine A to the treatment of Alzheimer's disease is discussed.

PMID:   11516831   [PubMed - indexed for MEDLINE]

The Essential Role of Hippocampal CA1 NMDA Receptor–Dependent Synaptic Plasticity in Spatial Memory

 

 

 

Summary We have produced a mouse strain in which the deletion of the NMDAR1 gene is restricted to the CA1 pyramidal cells of the hippocampus by using a new and general method that allows CA1-restricted gene knockout. The mutant mice grow into adulthood without obvious abnormalities. Adult mice lack NMDA receptor–mediated synaptic currents and long-term potentiation in the CA1 synapses and exhibit impaired spatial memory but unimpaired nonspatial learning. Our results strongly suggest that activity-dependent modifications of CA1 synapses, mediated by NMDA receptors, play an essential role in the acquisition of spatial memories.

NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD)

Edited by Area-1255, 22 September 2015 - 09:56 PM.

[nootist]

 

Any "natural" supplements for logic enhancing? Like Huoerzine, Tyrosine or Bacopa?

HuperZine A is also an NMDA antagonist; which may not be the best idea for logic/common sense. Seeing as how glutamate is necessary for logic and communication and Autistics are seen with deficits in glutamatergic transmission.

 

 

Then again, one of the autistic people I work with is an Applied Math/CS double major, who totally kills at most things which require pure logic.  Loves physics, chemistry, and a good game of chess.  Not that far from being a speech-delayed Sheldon Cooper.  Since hyperlexia and hypercalculia are almost exclusive to the autism spectrum, I find it puzzling that you would associate autism and defects in logic.  There are also a growing number of studies like this:

 

Child prodigies are rare individuals with an exceptional working memory and unique attentional skills that may facilitate the attainment of professional skill levels at an age well before what is observed in the general population. Some characteristics of prodigy have been observed to be quantitatively similar to those observed in autism spectrum disorder (ASD), suggesting possible shared etiology, though objectively validated prodigies are so rare that evidence has been sparse. We performed a family-based genome-wide linkage analysis on 5 nuclear and extended families to search for genetic loci that influence the presence of both prodigy and ASD, assuming that the two traits have the same genetic etiology in the analysis model in order to find shared loci. A shared locus on chromosome 1p31-q21 reached genome-wide significance with two extended family-based linkage methods consisting of the Bayesian PPL method and the LOD score maximized over the trait parameters (i.e., MOD), yielding a simulation-based empirical significance of p = 0.000742 and p = 0.000133, respectively. Within linkage regions, we performed association analysis and assessed if copy number variants could account for the linkage signal. No evidence of specificity for either the prodigy or the ASD trait was observed. This finding suggests that a locus on chromosome 1 increases the likelihood of both prodigy and autism in these families.

→ source (external link)

 

Most autistics have elevated serum glutamate, it's starting to look as if mGluR5 might be excessive, and there are questions about mGluR6.  I speculate that these may play a role in driving mGluR_2/3 down, but that's not exactly a generalized hypoglutamatergic state.  There has only been one paper in the last 8 years where the abstract includes both the words 'autism' and 'hypoglutamatergic,' and it found an NMDA antagonist (memantine) worked quite nicely on autistic kids.

 

Autism is a neurodevelopmental disorder that causes significant impairment in socialization and communication. It is also associated with ritualistic and stereotypical behaviour. Recent studies propose both hyper-and hypoglutamatergic ideologies for autism. The objective of this study was to assess the effects of memantine plus risperidone in the treatment of children with autism. Children with autism were randomly allocated to risperidone plus memantine or placebo plus risperidone for a 10-wk, double-blind, placebo-controlled study. The dose of risperidone was titrated up to 3 mg/d and memantine was titrated to 20 mg/d. Children were assessed at baseline and after 2, 4, 6, 8 and 10 wk of starting medication protocol. The primary outcome measure was the irritability subscale of Aberrant Behavior Checklist-Community (ABC-C). Difference between the two treatment arms was significant as the group that received memantine had greater reduction in ABC-C subscale scores for irritability, stereotypic behaviour and hyperactivity.

→ source (external link)

 

Apologies to the OP for hijacking the thread, but that one sentence bothered me, and I only had one post left in today's allotment.  Tomorrow I will try to get a grand unified autism theory thread started, so we can hash these things out in a more appropriate place.

[Area-1255]

Most autistics have elevated serum glutamate,

They do, really? Hm, that's interesting. So how do you explain this? 

 

 

 

Reduced subcortical glutamate/glutamine in adults with autism spectrum disorders: a [¹H]MRS study

 

 

Dysfunctional glutamatergic neurotransmission has been implicated in autism spectrum disorder (ASD). However, relatively few studies have directly measured brain glutamate in ASD adults, or related variation in glutamate to clinical phenotype. We therefore set out to investigate brain glutamate levels in adults with an ASD, comparing these to healthy controls and also comparing results between individuals at different points on the spectrum of symptom severity. We recruited 28 adults with ASD and 14 matched healthy controls. Of those with ASD, 15 fulfilled the ‘narrowly’ defined criteria for typical autism, whereas 13 met the ‘broader phenotype’. We measured the concentration of the combined glutamate and glutamine signal (Glx), and other important metabolites, using proton magnetic resonance spectroscopy in two brain regions implicated in ASD—the basal ganglia (including the head of caudate and the anterior putamen) and the dorsolateral prefrontal cortex—as well as in a parietal cortex ‘control’ region. Individuals with ASD had a significant decrease (P<0.001) in concentration of Glx in the basal ganglia, and this was true in both the ‘narrow’ and ‘broader’ phenotype. Also, within the ASD sample, reduced basal ganglia Glx was significantly correlated with increased impairment in social communication (P=0.013). In addition, there was a significant reduction in the concentration of other metabolites such as choline, creatine (Cr) and N-acetylaspartate (NAA) in the basal ganglia. In the dorsolateral prefrontal cortex, Cr and NAA were reduced (P<0.05), although Glx was not. There were no detectable differences in Glx, or any other metabolite, in the parietal lobe control region. There were no significant between-group differences in age, gender, IQ, voxel composition or data quality. In conclusion, individuals across the spectrum of ASD have regionally specific abnormalities in subcortical glutamatergic neurotransmission that are associated with variation in social development.

 

J Neural Transm. 1998;105(4-5):525-35.

Hypothesis: is infantile autism a hypoglutamatergic disorder? Relevance of glutamate - serotonin interactions for pharmacotherapy.

Carlsson ML1.

Author information

 

Abstract

Based on 1) neuroanatomical and neuroimaging studies indicating aberrations in brain regions that are rich in glutamate neurons and 2) similarities between symptoms produced by N-methyl-D-aspartate (NMDA) antagonists in healthy subjects and those seen in autism, it is proposed in the present paper that infantile autism is a hypoglutamatergic disorder. Possible future pharmacological interventions in autism are discussed in the light of the intimate interplay between central glutamate and serotonin, notably the serotonin (5-HT) 2A receptor. The possible benefit of treatment with glutamate agonists [e.g. agents acting on the modulatory glycine site of the NMDA receptor, or so-called ampakines acting on the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor] is discussed, as well as the potential usefulness of a selective 5-HT2A receptor antagonist.

PMID:   9720980   [PubMed - indexed for MEDLINE]

 

Edited by Area-1255, 23 September 2015 - 12:44 AM.

[platypus]

I think the two things that would help math/physics ability is improved visualization and improved working memory. The latter _might_ be helped by brain training, not sure what could increase the former but I suppose visualization exercises might help.  

[gamesguru]

Problem with lots of the research, is it's carried out with 105IQ ppl, not top level scientists or mathematicians, which would give us a different angle, and which the technology (fMRIs, etc) is ready for.

If you want to study higher order faculties, and ways to sharpen them, you have to push the limits.  We haven't quite designed tests to measure such faculties, yet.

 

http://www.longecity...okes-facts-etc/
http://www.longecity...fect-nootropic/

[Busyboy]

Any "natural" supplements for logic enhancing? Like Huoerzine, Tyrosine or Bacopa?

HuperZine A is also an NMDA antagonist; which may not be the best idea for logic/common sense. Seeing as how glutamate is necessary for logic and communication and Autistics are seen with deficits in glutamatergic transmission.

Neuroscience. 2001;105(3):663-9.Huperzine A, a nootropic alkaloid, inhibits N-methyl-D-aspartate-induced current in rat dissociated hippocampal neurons.
Zhang JM1, Hu GY.
Author information

Abstract

Huperzine A, a nootropic alkaloid isolated from a Chinese herb, has been proposed as one of the most promising agents to treat Alzheimer's disease. Recently, the agent was found to inhibit the N-methyl-D-aspartate (NMDA) receptors in rat cerebral cortex in addition to causing an inhibitory effect on acetylcholinesterase. In the present study, the mechanisms underlying NMDA receptor inhibition were investigated using whole-cell voltage-clamp recording in CA1 pyramidal neurons acutely dissociated from rat hippocampus. Huperzine A reversibly inhibited the NMDA-induced current (IC(50)=126 microM, Hill coefficient=0.92), whereas it had no effect on the current induced by alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate or kainate. The effect was non-competitive, and showed neither 'voltage-dependency', nor 'use-dependency'. The IC(50) values of huperzine A were neither altered by changing the concentrations of glycine (2-0.2 microM) and pH (7.4-6.7) in the external solution, nor by addition of Zn(2+) (5 microM) and dithiothreitol (5 mM) to the external solution. However, addition of spermine (200 microM) to the external solution caused a parallel shift to the right of the huperzine A concentration-response curve. From these we suggest that huperzine A acts as a non-competitive antagonist of the NMDA receptors, via a competitive interaction with one of the polyamine binding sites. The potential relevance of NMDA receptor antagonist activity of huperzine A to the treatment of Alzheimer's disease is discussed.

PMID: 11516831 [PubMed - indexed for MEDLINE]

The Essential Role of Hippocampal CA1 NMDA Receptor–Dependent Synaptic Plasticity in Spatial Memory

Summary We have produced a mouse strain in which the deletion of the NMDAR1 gene is restricted to the CA1 pyramidal cells of the hippocampus by using a new and general method that allows CA1-restricted gene knockout. The mutant mice grow into adulthood without obvious abnormalities. Adult mice lack NMDA receptor–mediated synaptic currents and long-term potentiation in the CA1 synapses and exhibit impaired spatial memory but unimpaired nonspatial learning. Our results strongly suggest that activity-dependent modifications of CA1 synapses, mediated by NMDA receptors, play an essential role in the acquisition of spatial memories.

NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD)

I take 50mcg of Huperzine A daily (excluding weekends). In your opinion, do you think this may actually worsen logic and comprehension of math, for example?

[Area-1255]

I take 50mcg of Huperzine A daily (excluding weekends). In your opinion, do you think this may actually worsen logic and comprehension of math, for example?

NMDAR antagonism helps with some aspects of intellectual function m8 but only long-term...activation helps with maintaining a balanced mind set. Activation is necessary to learn and dismiss fears whereas blocking the receptor promotes somewhat unwarranted fearlessness. In other words ; NMDA-glutamate complex allows for learned extinction of fears and helps with familiarity of such things due to increased visual cue processing and auditory retention...

 

Antagonism however, promotes sort of a dream-like state (evidenced by PCP and other NMDA antagonists that cause psychosis) - and mildly increases feelings of euphoria and even grandiosity but alas, can also increase paranoia ideations etc...

 

So it's a shift from logical thinking to not so logical thinking in terms of time and environment perception..with activation tending towards logic and 'remembering' key responses and say why 'this or that' should no longer be feared...antagonism basically creates personality changes and can lower heart rate etc... 

 

God forbid the guy who is on PCP and murders his whole family due to paranoia and the same with any glutamate-antagonist should be take under considering..as evidenced by schizophrenics whose main imbalance is decreased glutamate activity and function.

Consolidation of Fear Extinction Requires NMDA Receptor-Dependent Bursting in the Ventromedial Prefrontal Cortex

 

Extinction of fear-potentiated startle: blockade by infusion of an NMDA antagonist into the amygdala

 

NMDA receptor antagonism in the basolateral but not central amygdala blocks the extinction of Pavlovian fear conditioning in rats.

[Busyboy]

I take 50mcg of Huperzine A daily (excluding weekends). In your opinion, do you think this may actually worsen logic and comprehension of math, for example?

NMDAR antagonism helps with some aspects of intellectual function m8 but only long-term...activation helps with maintaining a balanced mind set. Activation is necessary to learn and dismiss fears whereas blocking the receptor promotes somewhat unwarranted fearlessness. In other words ; NMDA-glutamate complex allows for learned extinction of fears and helps with familiarity of such things due to increased visual cue processing and auditory retention...

Antagonism however, promotes sort of a dream-like state (evidenced by PCP and other NMDA antagonists that cause psychosis) - and mildly increases feelings of euphoria and even grandiosity but alas, can also increase paranoia ideations etc...

So it's a shift from logical thinking to not so logical thinking in terms of time and environment perception..with activation tending towards logic and 'remembering' key responses and say why 'this or that' should no longer be feared...antagonism basically creates personality changes and can lower heart rate etc...

God forbid the guy who is on PCP and murders his whole family due to paranoia and the same with any glutamate-antagonist should be take under considering..as evidenced by schizophrenics whose main imbalance is decreased glutamate activity and function. Consolidation of Fear Extinction Requires NMDA Receptor-Dependent Bursting in the Ventromedial Prefrontal Cortex
Extinction of fear-potentiated startle: blockade by infusion of an NMDA antagonist into the amygdala
NMDA receptor antagonism in the basolateral but not central amygdala blocks the extinction of Pavlovian fear conditioning in rats.

So how would you go about to "activate" the DA-glutamate complex thing? Is this something you can do with supplements or is it a mindset? Or are you just born with it? I'm sorry if I'm asking a silly question, I'm a total nube when it comes to this stuff :P

[Area-1255]

 

So how would you go about to "activate" the DA-glutamate complex thing? Is this something you can do with supplements or is it a mindset? Or are you just born with it? I'm sorry if I'm asking a silly question, I'm a total nube when it comes to this stuff :P

 

Noob* - and no it's good you are asking  questions... that's the only way we ever learn, really. 

I recommend a supplement called "Test Force II" - it's marketed as a testosterone booster but it's ingredients are purely DAA and Sarcosine which prevents the reuptake of glycine and co-activates the NMDAR - use that with a 'central potentiator' like Ashwagandha or nefiracetam. 

 

If you are trying to strengthen your resolve and NMDAR functions; don't use too much magnesium - although nefiracetam will stop magnesium's NMDA blocking effects , to an extent... also don't supplement with too much Zinc as this also works against NMDAR (generally, although if glutamate drops too low there is evidence Zn2+ can raise it to the right proportions)...

 

VERY IMPORTANT : If you take glutamatergics you MUST supplement a mild aromatase inhibitor WITH it - glutamate agonists are known to raise estrogen and in some cases prolactin - so they should only be administered with an AI... At least a strong natural one or something like Erase Pro or Triazole by Driven Sports.

 

Edited by Area-1255, 23 September 2015 - 11:50 PM.

[gamesguru]

I was reading this, the "polymath" guy says the g-factor is an attempt to weight together all mental faculties (of which there are apparently 8 major ones).

An illustration of John B. Carroll's three stratum theory, an influential contemporary model of cognitive abilities. The broad abilities recognized by the model are fluid intelligence (Gf), crystallized intelligence (Gc), general memory and learning (Gy), broad visual perception (Gv), broad auditory perception (Gu), broad retrieval ability (Gr), broad cognitive speediness (Gs), and processing speed (Gt). Carroll regarded the broad abilities as different "flavors" of g.

[baccheion]

Pramiracetam (spock-like logic, improves rote memorization ability)

N-Acetyl Semax (clear-headedness and fluidity)

PRL-8-53 (enhances short-term memory if you're a responder)

 

[Busyboy]

Pramiracetam (spock-like logic, improves rote memorization ability)
N-Acetyl Semax (clear-headedness and fluidity)
PRL-8-53 (enhances short-term memory if you're a responder)

I've been super interested in Pramiracetam but heard some users had memory problems when using it for months, which turned me off of it. May order it just to use periodically or when needed.

And what do you mean by spock-like logic? I know it numbs your emotions but how exactly does it help you for such great logic? Do you figure out complex things easier? Thanks

[baccheion]

 

Pramiracetam (spock-like logic, improves rote memorization ability)
N-Acetyl Semax (clear-headedness and fluidity)
PRL-8-53 (enhances short-term memory if you're a responder)

I've been super interested in Pramiracetam but heard some users had memory problems when using it for months, which turned me off of it. May order it just to use periodically or when needed.

And what do you mean by spock-like logic? I know it numbs your emotions but how exactly does it help you for such great logic? Do you figure out complex things easier? Thanks

 

Your emotions are numbed, so you become logical in a spock-like manner. Linear, logical reasoning becomes a lot easier.

Edited by baccheion, 25 September 2015 - 08:29 PM.

[Busyboy]

Has anyone used a specific nootropic that aided your comprehension and understanding of math or physics? I'm struggling in Advanced Calculus. Any help will be greatly appreciated

Edited by Busyboy, 21 October 2015 - 07:22 PM.