I'm not sure how much sulbutiamine has been discussed in these forums, but it's the active ingredient (apparently) in Biotest's Spike. In any event, for anyone who is interested there is some research indicating it has some use as a nootropic.
* Micheau J,
* Durkin TP,
* Destrade C,
* Rolland Y,
* Jaffard R.
Thiamine deficiency in both man and animals is known to produce memory dysfunction and cognitive disorders which have been related to an impairment of cholinergic activity. The present experiment was aimed at testing whether, inversely, chronic administration of large doses of sulbutiamine would have a facilitative effect on memory and would induce changes in central cholinergic activity. Accordingly mice received 300 mg/kg of sulbutiamine daily for 10 days. They were then submitted to an appetitive operant level press conditioning test. When compared to control subjects, sulbutiamine treated mice learned the task at the same rate in a single session but showed greatly improved performance when tested 24 hr after partial acquisition of the same task. Parallel neurochemical investigations showed that the treatment induced a slight (+ 10%) but significant increase in hippocampal sodium-dependent high affinity choline uptake. The present findings and previous results suggest that sulbutiamine improves memory formation and that this behavioral effect could be mediated by an increase in hippocampal cholinergic activity.
PMID: 4059305 [PubMed - indexed for MEDLINE]
Another rat study, this one indicating its (possible) psychopharmacological mode of action:
Author: Trovero, F : Gobbi, M : Weil Fuggaza, J : Besson, M J : Brochet, D : Pirot, S
Citation: Neurosci-Lett. 2000 Sep 29; 292(1): 49-53
Abstract: Chronic treatment of rats by sulbutiamine induced no change in density of N-methyl-D-aspartate (NMDA) and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors in the cingular cortex, but a significant decrease of the kainate binding sites, as measured by quantitative autoradiography. In the same treated animals, an increase of D1 dopaminergic (DA) binding sites was measured both in the prefrontal and the cingular cortex, while no modification of the D2 binding sites was detected. Furthermore, an acute sulbutiamine administration induced a decrease of kainate binding sites but no change of the density of D1 and D2 DA receptors. Acute sulbutiamine injection led to a decrease of the DA levels in the prefrontal cortex and 3,4-dihydroxyphenylacetic acid levels in both the cingular and the prefrontal cortex. These observations are discussed in terms of a modulatory effect of sulbutiamine on both dopaminergic and glutamatergic cortical transmissions.
Review References: None
Publication Type: Journal-Article
Now, if anyone could find human studies indicating its effectiveness, then we'd be getting somewhere. I don't buy into the hype which describes it as some sort of amphetamine-like high without the nasty side effects--but at least these two studies suggest it could have an empirically verifiable effect (if not only in mice, then possibly humans as well).