Oh come on guys! How about some science to back up what your saying. Heresay isn't good enough. If you are basing your claim on science then please reference it. This young man is going into a medical degree so he better get used to the evidence-based approach.
No Who-Ha please.
Anyhow......acetylcholine is the neurotransmitter that you should be concerned about when referring to energy. Hence, acetyl and choline donors may be effective. Addtionally, an acetylcholine esterase inhibitor such as Huperzine A may also help. Combine both donors and inhibitors are you should be on the right track.
Keep in mind though that most therapeutics are exactly that, therapeutics. Devices to treat an already compromised situation.
Ann N Y Acad Sci. 2004 Nov;1033:108-16.Click here to read Links
Delaying the mitochondrial decay of aging with acetylcarnitine.
Ames BN, Liu J.
Nutritional Genomics Center, Children's Hospital Oakland Research Institute, Oakland, CA 94609, USA. bames@chori.org
Oxidative mitochondrial decay is a major contributor to aging. Some of this decay can be reversed in old rats by feeding them normal mitochondrial metabolites, acetylcarnitine (ALC) and lipoic acid (LA), at high levels. Feeding the substrate ALC with LA, a mitochondrial antioxidant, restores the velocity of the reaction (K(m)) for ALC transferase and mitochondrial function. The principle appears to be that, with age, increased oxidative damage to protein causes a deformation of structure of key enzymes with a consequent lessening of affinity (K(m)) for the enzyme substrate. The effect of age on the enzyme-binding affinity can be mimicked by reacting it with malondialdehyde (a lipid peroxidation product that increases with age). In old rats (vs. young rats), mitochondrial membrane potential, cardiolipin level, respiratory control ratio, and cellular O(2) uptake are lower; oxidants/O(2), neuron RNA oxidation, and mutagenic aldehydes from lipid peroxidation are higher. Ambulatory activity and cognition decline with age. Feeding old rats ALC with LA for a few weeks restores mitochondrial function; lowers oxidants, neuron RNA oxidation, and mutagenic aldehydes; and increases rat ambulatory activity and cognition (as assayed with the Skinner box and Morris water maze). A recent meta-analysis of 21 double-blind clinical trials of ALC in the treatment of mild cognitive impairment and mild Alzheimer's disease showed significant efficacy vs. placebo. A meta-analysis of 4 clinical trials of LA for treatment of neuropathic deficits in diabetes showed significant efficacy vs. placebo.
Methods Find Exp Clin Pharmacol. 2006 Sep;28 Suppl B:1-56.Click here to read Links
Citicoline: pharmacological and clinical review, 2006 update.
Secades JJ, Lorenzo JL.
Medical Department, Grupo Ferrer S.A., Barcelona, Spain.
Cytidine 5'-diphosphocholine, CDP-choline, or citicoline is an essential intermediate in the biosynthetic pathway of structural phospholipids in cell membranes, particularly phosphatidylcholine. Following administration by both the oral and parenteral routes, citicoline releases its two main components, cytidine and choline. Absorption by the oral route is virtually complete, and bioavailability by the oral route is therefore approximately the same as by the intravenous route. Once absorbed, citicoline is widely distributed throughout the body, crosses the blood-brain barrier and reaches the central nervous system (CNS), where it is incorporated into the membrane and microsomal phospholipid fraction. Citicoline activates biosynthesis of structural phospholipids of neuronal membranes, increases brain metabolism, and acts upon the levels of different neurotransmitters. Thus, citicoline has been experimentally shown to increase norepinephrine and dopamine levels in the CNS. Owing to these pharmacological mechanisms, citicoline has a neuroprotective effect in hypoxic and ischemic conditions, decreasing the volume of ischemic lesion, and also improves learning and memory performance in animal models of brain aging. In addition, citicoline has been shown to restore the activity of mitochondrial ATPase and membrane Na+/K+ATPase, to inhibit activation of certain phospholipases, and to accelerate reabsorption of cerebral edema in various experimental models. Citicoline has also been shown to be able to inhibit mechanisms of apoptosis associated to cerebral ischemia and in certain neurodegeneration models, and to potentiate neuroplasticity mechanisms. Citicoline is a safe drug, as shown by the toxicological tests conducted, that has no significant systemic cholinergic effects and is a well tolerated product. These pharmacological characteristics and the action mechanisms of citicoline suggest that this product may be indicated for treatment of cerebral vascular disease, head trauma (HT) of varying severity, and cognitive disorders of different causes. In studies conducted in the treatment of patients with HT, citicoline was able to accelerate recovery from post-traumatic coma and neurological deficits, achieving an improved final functional outcome, and to shorten hospital stay in these patients. Citicoline also improved the mnesic and cognitive disorders seen after HT of minor severity that constitute the so-called post-concussional syndrome. In the treatment of patients with acute ischemic cerebral vascular disease, citicoline accelerates recovery of consciousness and motor deficit, achieves a better final outcome, and facilitates rehabilitation of these patients. The other major indication of citicoline is for treatment of senile cognitive impairment, either secondary to degenerative diseases (e.g. Alzheimer disease) or to chronic cerebral vascular disease. In patients with chronic cerebral ischemia, citicoline improves scores in cognitive rating scales, while in patients with senile dementia of the Alzheimer type it stops the course of disease, and neuroendocrine, neuroimmunomodulatory, and neurophysiological benefits have been reported. Citicoline has also been shown to be effective in Parkinson disease, drug addictions, and alcoholism, as well as in amblyopia and glaucoma. No serious side effects have occurred in any series of patients treated with citicoline, which attests to the safety of treatment with citicoline. © 2006 Prous Science. All rights reserved.
Trends Pharmacol Sci. 2006 Dec;27(12):619-25. Epub 2006 Oct 23.Click here to read Links
Neuroprotective effects of huperzine A: new therapeutic targets for neurodegenerative disease.
Zhang HY, Tang XC.
State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhangjiang Hi-Tech Park, Shanghai 201203, China.
In recent years, the most common pharmacological treatment for Alzheimer's disease (AD) has been acetylcholinesterase (AChE) inhibition. However, this single-target approach has limited effectiveness and there is evidence that a multitarget approach might be more effective. Huperzine A (HupA), a novel alkaloid isolated from a Chinese herb, has neuroprotective effects that go beyond the inhibition of AChE. Recent data have demonstrated that HupA can ameliorate the learning and memory deficiency in animal models and AD patients. Its potentially beneficial actions include modification of beta-amyloid peptide processing, reduction of oxidative stress, neuronal protection against apoptosis, and regulation of the expression and secretion of nerve growth factor (NGF) and NGF signaling.
Re. an anti-stress compound....well I prefer Rhodiola over bacopa. The research on bacopa generally suggests that you require chronic dosing for about 12 weeks before you see an effect on memory. Rhodiola on the otherhand has almost immediate effects with a generous 8 hour or so half life per 500mg (5% rosavins)
Phytother Res. 2005 Oct;19(10):819-38.
Stimulating effect of adaptogens: an overview with particular reference to their efficacy following single dose administration.
Panossian A, Wagner H.
Swedish Herbal Institute, Viktor Rydbergsgatan 10, SE-411 32 Gothenburg, Sweden. ap@shi.se
Plant adaptogens are compounds that increase the ability of an organism to adapt to environmental factors and to avoid damage from such factors. The beneficial effects of multi-dose administration of adaptogens are mainly associated with the hypothalamic-pituitary-adrenal (HPA) axis, a part of the stress-system that is believed to play a primary role in the reactions of the body to repeated stress and adaptation. In contrast, the single dose application of adaptogens is important in situations that require a rapid response to tension or to a stressful situation. In this case, the effects of the adaptogens are associated with another part of the stress-system, namely, the sympatho-adrenal-system (SAS), that provides a rapid response mechanism mainly to control the acute reaction of the organism to a stressor. This review focuses primarily on the SAS-mediated stimulating effects of single doses of adaptogens derived from Rhodiola rosea, Schizandra chinensis and Eleutherococcus senticosus. The use of these drugs typically generates no side effects, unlike traditional stimulants that possess addiction, tolerance and abuse potential, produce a negative effect on sleep structure, and cause rebound hypersomnolence or 'come down' effects. Furthermore, single administration of these adaptogens effectively increases mental performance and physical working capacity in humans. R. rosea is the most active of the three plant adaptogens producing, within 30 min of administration, a stimulating effect that continues for at least 4-6 h. The active principles of the three plants that exhibit single dose stimulating effects are glycosides of phenylpropane- and phenylethane-based phenolic compounds such as salidroside, rosavin, syringin and triandrin, the latter being the most active. Copyright © 2005 John Wiley & Sons, Ltd.
Vinpocetine.....?? yeah ....nah.....jury is still out IMO re. the effects in healthy individuals (see attached monograph)
Most of what dopamine said
Add one ingredient at a time slowly to gauge your response, nootropics can have contradictory effects at the wrong doses. Sulbutiamine is indicated for anergia (lack of energy), but Bacopa and L-Theanine generally have "anti-stress" effects that some simultaneously find sedating, and therefore counterproductive for your purposes (unless you have a problem with stress, in which case they could prove effective). Acetylcarnitine and alpha gpc are cholinergic, and may produce associated side-effects (usually head or neck tension), so take the lowest dose and move upwards unless you run into unpleasant effects. R-ALA is a good antioxidant, but probably won't help with focus or attention span in school. Piracetam is cheap and many find it effective in an academic setting, myself included, and is probably best suited for what you are looking for.
is good advice especially the part about taking it step by step.
Re. energy.....again, try and manipulate the neurotransmitters involved in energy. For example, D,L-Phenylalanine is a great dopamine precursor. Take this on an empty stomach away from other Large Neutral Amino Acids (LNAAs). Chocamine will add an extra boost.
Edited by zoolander, 30 April 2008 - 05:49 AM.
