Individual requirements can vary all over the board for some things. Frequently northern-European peoples need many times the RDA of certain B vitamins. Others may have adverse reactions to megadoses of these (I am one.)
Do you think it's a cholinergic effect? Cholinergic excess causes
irritability, you reported anger from excessive B1 or B2, and the following papers show cholinergic effects from these vitamins. (Yeah, I admit the B2 paper is a bit of a stretch, but B1 is definitely implicated.)
I think Deprenyl tablet rage might be cholinergic too. Edward reported cholinergic symptoms like edema and jaw and neck tension accompanying his irritability.
Ann Neurol. 1993 Nov;34(5):724-6.
Evidence for a central cholinergic effect of high-dose thiamine.
Meador KJ, Nichols ME, Franke P, Durkin MW, Oberzan RL, Moore EE, Loring DW.
Department of Neurology, Medical College of Georgia, Augusta 30912-3280.
In vitro animal studies have suggested that thiamine is involved in the presynaptic release of acetylcholine. Total thiamine content in cholinergic nerve terminals is comparable with that of acetylcholine, and the phosphorylation state of thiamine changes with release of acetylcholine. Thiamine binds to nicotinic receptors and may exhibit anticholinesterase activity. Based on these observations, we investigated the effects of pharmacological doses of thiamine on the cognitive deficits induced by the anticholinergic scopolamine in healthy young adults using a randomized, double-blind, placebo-controlled, double-crossover design. Drug effects were assessed by P3 event-related potential, quantitated electroencephalography, and free recall memory. Conditions included (1) baseline, (2) thiamine 5 gm p.o. and scopolamine 0.007 mg/kg IM, and (3) lactose PO and scopolamine 0.007 mg/kg IM. Thiamine significantly reduced adverse effects of scopolamine on P3 latency, spectral components of electroencephalography, and memory recall. The results are consistent with a cholinomimetic effect of thiamine in the central nervous system. Additional studies are needed to delineate the basic mechanisms and possible therapeutic efficacy of thiamine at pharmacological dosages.
PMID: 8239567
Can J Physiol Pharmacol. 1997 May;75(5):423-30.
Decompensation of hepatic and cerebral acyl-CoA metabolism in BALB/cByJ mice by chronic riboflavin deficiency: restoration by acetyl-L-carnitine.
Rao KV, Qureshi IA.
Division of Medical Genetics, Hõpital Sainte-Justine, University of Montréal, QC, Canada.
BALB/cByJ mice have an autosomal recessive deficiency of short-chain acyl-CoA dehydrogenase (SCAD) and show elevated excretion of urinary butyrylglycine, ethylmalonate, and methylsuccinate, which resembles the SCAD deficiency disorder in children. These mice are clinically normal, perhaps because of an efficient acyl-CoA conjugation system. We attempted to decompensate the acyl-CoA metabolism in mutant mice by chronic treatment with a riboflavin-deficient diet for 3 weeks to potentiate the SCAD deficiency. We studied the urinary profiles of organic acids, acylglycines, hepatic and cerebral profiles of carnitines, and ammonia to assess the potentiation of this disorder. Cerebral activity of choline acetyltransferase (ChAT) was determined to study the effects of acyl-CoA accumulation on the cholinergic system. The results indicate that in riboflavin-deficient mutant mice, the excretion of ethylmalonate, methylsuccinate, butyrylglycine, and dicarboxylic acids was enhanced. Hepatic and cerebral free and esterified carnitines were reduced, indicating a potentiation of the secondary carnitine deficiency. Hepatic ammonia levels, but not cerebral ammonia or glutamine levels, were elevated, indicating a tendency towards secondary hyperammonemia. Brain choline acetyltransferase activity was significantly reduced in striatum, implying a reduced availability of cerebral acetyl-CoA or a decreased cerebral transport of choline: Most of these changes were partially or completely restored by a concomitant treatment with acetyl-L-carnitine (ALCAR). In summary, we conclude that BALB/cByJ mice with SCAD deficiency, but with a functional urea cycle, might have an adequate adaptive mechanism to adjust to an excessive acyl-CoA load without hyperammonemia at the cerebral level. However, any deficiency of vitamins or cofactors in the diet could disturb an adaptation to this disorder and produce an effect on the cholinergic system.
PMID: 9250376