here's the abstract from a study I found:
Cognitive enhancing substances such as amphetamine and modafinil have become popular in recent years to improve acute cognitive performance particularly in environments in which enhanced cognition or intelligence is required. Nutraceutical nootropics, which are natural substances that have the ability to bring about acute or chronic changes in cognition have also been gaining popularity in a range of settings and applications including the workplace, driving and in the amelioration of age related cognitive decline. Huperzine A, Vinpocetine, Acetyl-L-carnitine, Rhodiola Rosea and Alpha-lipoic Acid are popular nutritional supplements that have shown promising benefits in improving a range of biological (e.g., blood flow, anti-inflammatory, anti-oxidant, and direct neurotransmitter effects) and cognitive processes from in vitro, animal and human clinical research. We report here the first human randomized clinical trial for cognition in which we administer a combination of Huperzine A, Vinpocetine, Acetyl-carnitine, R Rosea and Alpha-lipoic acid (called Ceretrophin) vs placebo. Sixty participants (40 females and 20 males, with a mean age of 45.4 years, SD = 12.6) completed either the odd or even items from the Raven Advanced Progressive Matrices (APM) at baseline and the opposite odd or even items at week 4 after consuming either the combination nootropic or placebo. A significant study visit (time) x treatment condition interaction wasfound: F (1, 57) = 7.279, p = 0.009, partial eta(2) = .113, with paired samples t-tests revealing a significant improvement in mean APM score from baseline to retest (week 4) (t(34) = -4.045, p <.001) for the Ceretrophin (TM) group. Improvements in APM scores could be attributed to the active intervention over the placebo, indicating that the treatment improved general intelligence. Implications for improving our understanding of the biological basis of intelligence and pharmacologically improving human cognition are discussed
nearly three decades have now passed since the discovery of the piracetam-like nootropics, compounds which exhibit cognition-enhancing properties, but for which no commonly accepted mechanism of action has been established. This review covers clinical, pharmacokinetic, biochemical and behavioural results presented in the literature from 1965 through 1992 (407 references) of piracetam, oxiracetam, pramiracetam, etiracetam, nefiracetam, aniracetam and rolziracetam and their structural analogues. The piracetam-like nootropics are capable of achieving reversal of amnesia induced by, e.g., scopolamine, electroconvulsive shock and hypolda. Protection against barbiturate intoxication is observed and some benefit in clinical studies with patients suffering from mild to moderate degrees of dementia has been demonstrated. No affinity for the alpha(1)-, alpha(2)-, beta-, muscarinic, 5-hydroxytryptamine-, dopamine, adenosine-A(1)-, mu-opiate, gamma-aminobutyric acid (GABA) (except for nefiracetam (GABA(A))), benzodiazepine and glutamate receptors has been found. The racetams possess a very low toxicity and lack serious side effects. Increased turnover of different neurotransmitters has been observed as well as other biochemical findings, e.g., inhibition of enzymes such as prolylendopeptidase. So far, no generally accepted,mechanism of action has, however, emerged. We believe that the effect of the racetams is due to a potentiation of already present neurotransmission and that much evidence points in the direction of a modulated ion flux by, e.g., potentiated calcium influx through non-L-type voltage-dependent calcium channels, potentiated sodium influx through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor gated channels or voltage-dependent channels or decreases in potassium efflux. Effects on carrier mediated ion transport are also possible.
bit too sciencey that one, but the gist seems to be they work (albeit just a little) and have low toxicity and side effects.