Combinations - Adderall + Nootropic Stack

[Dr.Evil]

Before I begin with this question for SWIM, I would like to say that the main question will most likely (prove me wrong) only be able to be answered accurately by a pharmacologist, or someone with universty/professional knowledge, but SWIM wants to know what everyone thinks. To save time and length I will use common abbreviations for enzymes, neurotransmitters, and several nootropics. That being said I know I'm a noob (OMG h4xorz! LOL! ) so at the end of the post I will list out the full names of each next to the abbreviations like it says to in the rules.

Background Info

SWIM is a 4th year University student who is studying to get into evil medical school. SWIM has been taking Adderall/Ritalin for a couple of years to study for classes. SWIM doesn't need Adderall to study, and has found that it actually impedes his learning in several courses (organic chemistry, creative writing, etc..), but greatly enhances intense memorization (biology, physics, etc..). This is what SWIM needs now, intense memorization and recall, and SWIM would like to know what people think of this stack in combination with Adderall for ~30 days. SWIM also happens to be a regular smoker and coffee drinker.

Drug/Dosage Info

Adderall 20mg - total 12.6 mg AMPH equiv.

Vitamins/other
210 mg Vitamin C, 15 mg Vitamin B-6, 800 mcg Folic Acid, 48 mcg Vitamin B-12, 330 mcg Biotin, 5 mg Pantothenic Acid, 75 IU Vitamin E, 3500 IU Vitamin A, 400 IU Vitamin D, 20 mcg Vitamin K, 1.2 mg Thiamin (B1), 1.7 mg Riboflavin (B2), 16 mg Niacin.---also various small amounts of elements (calcium, copper, selenium, potassium,etc...)


*note-- SWIM ingests the Vitamins/Nootropic Stack ~2 hrs after the Adderall to minimze the loss of absorption. (Acidifying agents such as Vitamin C and Glutamic Acid decrease Adderall absorption)

Nootropic Stack

Soy Lecithin 200 mg-- increases overall choline/ACh levels

EPA 150 mg-- precursor to DHA, inhibitory effect on several CYP liver enzymes

DHA 100 mg-- most abundant poly-unsaturated fatty acid in CNS

Acetyl L-Carnitine 50mg-- shown to have neuroprotective properties (in animal models) and believed to have a higher bioavailability than L-carnitine

Huperzine A 100 mcg-- AChE inhibitor, and NMDA receptor antagonist (protects from GLU induced damage from hyperexcitation of neurons, and increases nerve growth factor?)

Vinpocetine 5 mg-- correlation with neuronal protection effects, PDE-1 inhibitor= increased levels of 2nd messenger cGMP, which is believed to lead to vasorelaxant effects (increased cerebral blood flow) , and has been shown to increase neuronal levels of DOPAC which is a metabolite of DA.

Alpha Lipoic Acid 100 mg, Ginko Bilboa Extract 120 mg, Gotu Kola Extract 30 mg

Blend totalling 86.22 mg of the following

Phosphatidylserine-- blunts stress induced increases in cortisol levels, which have been shown to have neurodegenerative effects

DMAE-- thought to be ACh precursor, known to be processed by liver into choline, but cannot pass the blood brain barrier.

L-Glutamic Acid-- direct precursor for the NT (neurotransmitter) glutamate which stimulates NMDA receptors.

Inositol-- precursor for all PI based 2nd messengers (PIP,PIP2, PIP3) which helps regulate intracellular Ca2+ concentration and therefore membrane potential.

Questions/Concerns

SWIM would first of all like to know what people think of this stack, and if anyone has info on the items listed that don't have added benefit besides being something the body needs (things listed without description).

Adderall is believed to work by inhibiting reuptake, and increasing release of DA and NE. ---Question 1--does Adderall have any effect on ACh?

As stated above, some of the above compounds are believed to increase precursor levels for DA (Vinpocentine) and NE (synthesized from DA). Adderall by itself inhibits MAO-A/B, which increases DA/NE. Also because SWIM is a smoker, near constant nicotine exposure agonizes the nAChR's which in turn leads to a further increase in DA in certain brain regions (specifically the nucleus accumbens, or NAc).
--Question 2-- Should SWIM cycle this stack? Swim isn't sure what a normal cycle could be, and is wondering if the constant increases in NT's (without off-time) could lead to a down-regulation of the DA/NE receptors, which in turn would basically cancel the effects of the stack.

Many of these nootropic compounds affect the NT ACh. Huperzine A is an AChE inhitbitor, which means less ACh breakdown. Soy Lecithin (phosphatidylcholine) leads to an increase in choline and therefore ACh. DMAE is also thought to be a precursor to ACh. So exactly as in question 2 should this be cycled to avoid a down-regulation of ACh receptors? and if so how should it be cycled?

Last but not least, SWIM wants to enhance the brains LTP response (long-term potentiation). LTP is believed to be a key component of long-term memory and cognition. In a nutshell, LTP happens by strong activation of NMDA receptors, which in turn leads to that and other receptors being up-regulated and increasing there activity. L-Glutamic Acid as stated above causes an increase in the NT glutamate which stimulates the NMDA receptor, Inositol increases 2nd messenger systems which are critical for an increase in Ca2+ that is the next step after NMDA receptor activation. Huperzine A is a NMDA receptor antagonist that blocks activation of the NMDA receptors by glutamate (this would normally would cause an up-regulation of the receptors thereby increasing the chance for LTP, but the extra glutamate via L-Glutamic acid might offest this??)

--Question 3-- Does anyone believe this will in fact increase SWIM's LTP response? and once again, should it be cycled as to not over-stimulate the receptors causing a down-regulation.

Also does anyone know what would be considered a "high-dose" of EPA, because it has been shown to inhibit CYP2D6/3A4 which are some of the liver isozymes that metabolize Adderall??

Abbreviations

ACh--Acetylcholine
AChE-- Acetylcholine esterase (breaks down ACh)
nAChR-- nicotinic Acetylcholine receptors
NMDA-- N-methyl-D-aspartate receptors (activated by glutamate)
DA-- Dopamine
NE-- Norepinephrine
MAO(A/B)-- Monoamine oxidase A or B (breaks down DA and NE)
EPA-- Eicosapentaenoic acid
DHA-- Docosahexaenoic acid
CYP-- Cytochrome P (liver enzymes responsible for majority of drug metabolism)
DOPAC-- 3,4-Dihydroxyphenylacetic acid (metabolite of DA)
PI-- Phosphatidylinositol
cGMP-- cyclic guanine monophosphate (2nd messenger)
PDE1--phosphodiesterase type-1 inhibitor (causes increased cGMP levels)
DMAE- dimethylethanolamine

Sorry for the length, hopefully I can find SWIM some answers so he can become the evil doctor he has always wanted to be!

Reputation Comments on this post:

Interesting and well explained question.