Although I hate generalizing, with science (or really neurobiology) there comes a time where consistency in rapport (between studies and researchers) leads to comfortability. Oh there comes a time when we need the most straightforward, fairly simple consistencies to elevate our understanding of such things.
Well, now is that time.
:: :: :: VITAMINS :: :: ::
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Vitamin A: Decreases acetylcholine synthesis (except when correcting deficiency)(1)(2), increases growth factors and essential to maturation of hippocampus and other important brain regions(3), protects against beta-amyloid in the brain(4), maintains dopamine D(2) receptor expression(5).
Vitamin B1 (THIAMINE) : essential to forming serotonin-ergic neuronal networks/mossy fibres and to maintaining integrity of glutamate-networks(6)(7), increases acetylcholine and corrects acetylcholine deficiency(8)(9)(10), increases dopamine in the striatum(11), modulates/inhibits serotonin synthesis(12), essential to brain norepinephrine function and cognitive processes(13)(14), necessary for both glutamate and GABA production(15).
Vitamin B2 (RIBOFLAVIN) : affects sensitivity of the MAO-A enzyme to inhibition(16), increases acetylcholine at high doses but does not affect at low doses(17), decreases glutamate from cortical nerves(18). may improve some symptoms of ADD by impacting central alpha & beta wave performance(19)
Vitamin B3 : may increase histamine and serotonin as well as nitric oxide levels(20)(21), increases BDNF and may improve brain cell growth(22).
Vitamin C : (ascorbic acid/ascorbate) ; decreases striatal dopamine(6), increases norepinephrine production from dopamine(7)(8), increases acetylcholine at high doses(9)(10), protects against NMDA and glutamate related cell death(11)(12), decreases histamine release(13)(14), necessary for serotonin synthesis(15), necessary for dopamine production(16).
Vitamin D - Increases serotonin production rates and general serotonin synthesis (17)(18) as well as dopamine synthesis(19) (formation), protects against glutamate neurotoxicity(20), inhibits inducible nitric oxide synthase which may reduce inflammation and cell death(21), does not notably reduce other forms of nitric oxide however, increases glutathione and concentrations of antioxidant enzymes(22), necessary for glutamate decarboxylase (GAD) which is responsible for converting Glutamate into GABA; meaning Vitamin D is essential for creating GABA and moderating glutamate exposure(23), Vitamin D regulates muscarinic 3 receptor expression and prevents excess expression in Diabetes (24), decreases acetylcholine in high doses(25).
Vitamin E : increases acetylcholine release at low or high doses (26 ), attenuates/decreases excitotoxicity/protects against excess glutamate effect on neurons(27), increases glutamate when low, prevents excess GABA accumulation(28)
Vitamin K : decreases acetylcholine in low or high doses (29), regulates cell proliferation in olfactory bulb inputs and subventricular stem cells(30), maintains normal insulin sensitivity and helps offset diabetes (31), necessary for protein production in human hypothalamus, hippocampus, pons medulla and other brain regions - and helps maintain . increase mitochondrial energy production(32)(33)(34)(35).
Iron : Essential for glutamate binding and GABA transaminase activities( ).
Increases nAChR's (nicotinic-Acetylcholine-Receptors) and massively increases NMDA-Receptors in Hippocampus (!) (!!)
Iron is also needed for TH and TPH as well as both monoamine oxidases; thus , IRON is necessary for production of DOPAMINE, SEROTONIN, glutamate AND GABA as well as the breakdown of the former two (*!!!*)
Magnesium : Necessary for 5-HT(1)A Serotonin Receptor Expression (!) (!!) (!!!) (!!!!)
Blocks NMDA Receptors (!!!!!)
Zinc(Zn): negative allosteric modulator of 5-HT1A receptors and signaling; may improve memory theoretically by lessening inhibitory serotonin influence( ), negative allosteric modulator of GABA-(A) function; this may explain anxiogenic effects of high dose Zinc therapy, however, it also may explain it's memory and synaptic improving events(!).
Zinc amplifies and induces supersensitivity of MUSCARINIC acetylcholine Receptors; in part by upregulating the receptors in all major brain regions..thus , Zinc is essential for maintenance of Acetylcholine-receptor function and can be categorized as one of the major minerals involved in receptor expression. {<see here>}
- Zinc also amplifies and potentiates Beta-2-Adrenoreceptors (B2) by acting as a PAS (Positive Allosteric Modulator) ; this means Zinc (Zn2+) can improve the efficacy / benefits of ASTHMA Medications that use this pathway (ALBUTEROL, CLENBUTEROL, FORMOTEROL etc)... (<see here>)
- CAUTION: Moderate-High dose Zinc is then expected to also INCREASE one's sensitivity to BOTH Caffeine and Albuterol / other asthma drugs that act as BETA-AGONISTS.
ZINC is involved in NMDA-Receptor regulation; it blocks the uptake of Glutamate and Aspartate into the HIPPOCAMPUS (~*~) and directly blocks NMDA-Receptors (*C-Here*)
tags :: NMDA-receptor binding, glutamate ion channels, minerals affecting glutamate neurotransmission, minerals affecting n.o synthesis, minerals affecting histamine, nos free radicals, the effects of zinc on l-glutamate binding, effects on serotonin receptors by minerals,
