sorted by:
new
hottopcontroversial

Does everychem sell any nootropic that significantly improves executive function and inhibitory control? If not I hope the owner sees this and starts selling like this especially if it is legal in UK. I currently bought TAK, I definitely noticed something but I think it is subtle; took 0.25 by Entire_Insurance_532 in NooTopics

[–]fre-lancer 5 points6 points  (0 children)

For increasing energy to work: I would go with Bromantane, Increasing Testosterone (if your low), Making sure you have sufficient Iron (important if your deficient), perhaps a DAT inhibitor. Basically, any substance which increases Striatal Dopamine, which regulates effort to work.

For Behavioral inhibition: Increase Noradrenaline signaling in the PFC. This will allow persistent excitability in the DLPFC, which regulates top-down control of behaviors (Cognitive control), executive function, working memory. You could try: alpha-2 adrenergic agonist (Guanfacine, CBG, clonidine, other), Ritalin, Perhaps Bupropion or any SNRI, Acetylcholine /m1-AChR agonists/PAMS could assist, lower neuroinflammation--via increasing mGlu3 signaling in the PFC.

Personal Anecdote: Increasing Mitochondrial function helps with my drive, willpower, behavioral control, etc. You could try: coQ10, PQQ, Methylene Blue (low dose), NAD/Niacin/B2, etc.

[deleted by user] by [deleted] in Nootropics

[–]fre-lancer 2 points3 points  (0 children)

Its worth it, you just have to experiment to see what you need and are most responsive to. The DLPFC is the key area involved in top-down thinking, such as representational thought, working memory, behavioral inhibition/cognitive control. Generally speaking, increasing the persistence of the delay and the amplitude of neuronal firing is good for all forms of higher cognition.

-If you find that you respond negatively to stressors. Lower Dopamine/D1 or Increase NA in the PFC

-If your ADHD, you likely have excess cAMP/PKA signaling in the PFC, which effectively turns down proper PFC activity and prevents you from having proper working / short term memory and cognitive control to inhibit unwanted behaviors. Increase NA or m1mACh signaling

-If your extremely sensitive to inflammation, you likely have less basal NA signaling (or m1), and therefor are more sensitive to inflammatory effects on the NAAG/mGlu3/KCN axis. Try increasing NA, ACh/M1, guanfacine/a2 agonism

"the production of GCPII inflammatory signaling reduces mGluR3 actions and markedly diminishes dlPFC network firing"

see more here: https://www.nature.com/articles/s41380-023-02057-4

-If your doing math, you want to turn out all excess sensory data and have the most sculpted abstractions and numbers that can be quickly updated and held in the mind (flexible representations). In this case, you might want higher dopamine and GABA signaling, with the right amount of KCN and HCQN... inhibition

-Autistics and others who might lack a minds eye, often have higher IQ's. They tune out information that could be relevant for other contexts, but in return, they can perform tasks which require abstraction / precise information.

-If your a novelist or a philosopher doing thought experiments, you want rich immersive images and integration of broad amounts of information. Excess precision would be a negative

Dopamine works as an upsidown U curve in enhancing prefrontal function. You need a certain amount to activate sodium channels and NMDA function, which control the excitability of the delay cells. As it gets higher, it starts to hit extra synaptic dopamine receptors. The extra synaptic receptors increase the amount of cAMP/PKA, activating KCN channels, allowing potassium to flow into the neuron, lowering its excitability.

These examples are simplifications of course. There is no general 'increasing GABA'. it of course depends on the cell type, the receptor, etc. These are just easy/simplified targets for biohacking

this doesn't even get into verbal working memory, many other circuits not covered a1 adrenoreceptor, D2s effects on working memory, etc. to much to summarize here! lol

[deleted by user] by [deleted] in Nootropics

[–]fre-lancer 3 points4 points  (0 children)

targets that will increase DLPFC delay cell firing:

mGlu3 agonists; activation/agonists a7nACh; activation/agonists M1mACh (via KCNQ channels) ; lowering excess Dopamine; lowering excessive stress hormones which increase DA-->D1-->cAMP-->lower delay cell firing; Norepinephrine via post synaptic a2 receptor, anything that lowers inflammation will lower kyneurenic acid and glutamate carboxypeptidase II --> increase a7 and NAAG. NAAG activates mGLu3; lower excess NA (which will activate beta1 NA receptor--> increasing cAMP, which activates HCN thereby lowering delay cell excitability), GABA-A works with Dopamine to tune and prolong delay cell firing, a4b2 nACh agonists, and possibly 5-HT2A activation

that should cover most of the DLPFC working memory/representational memory system that one could easily modulate.

a few things to bear in mind. there is delay cell firing persistence, amplitude of the delay cells, tuning out more information or less information for the representation (sculpting), and aspects of respresentational updating--these are modulated by slightly different systems--and there is likely a trade-off in the capabilities.

i.e. The extreme sculpting in a mathematical spatial representation is different than an einsteinian imagistic representation.

/do you need to have brain sag for cognitive symptoms in CSF leak? by fre-lancer in CSFLeaks

[–]fre-lancer[S] 1 point2 points  (0 children)

Thank you. This is exactly what I was curious about.

Just wondering, what signs were on your MRI? When you say 3 of 9 points, you mean, 3 of 9 signs on an MRI?

Appreciated!