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BodyQUICKEN

BodyQUICKEN

Does anybody here know anything about this? It’s supposed to increase activity level, among other things.

It contains
* Phosphatidylserine

* Huperzine-A

* Vinpocetine

* Niacinamide

* Thioctic Acid

* 2-Dimethylaminoethanol

* Contains no ephedrine, yohimbine HCL, or other dangerous ingredients.

http://www.sherdog.bigstep.com/item…00&PRID=1263187


Tex3

"Sadly, however, seconds after its launch, it undergoes SMEF, or Spontaneous Massive Existence Failure,and disappears." Douglas Adams

Vinpocetine

WHAT IS IT?
Vinpocetine, sometimes called Cavinton, is derived from vincamine, an extract of the periwinkle plant, Criocerus longiflorus.

WHAT DOES IT DO?
Vinpocetine is a marvelously effective memory enhancer. It increases the metabolism of the brain several ways. It increases blood flow to the brain, it increases the ATP production rate of the brain (ATP is the energy currency of the brain), and it speeds up the use of oxygen and glucose in the brain.
It also increases the brain’s tolerance to a lack of oxygen, which may be important for mountain climbers, divers, and those about to be operated on. Among its other properties is lessening platelet stickiness (to prevent strokes and heart attacks) and increasing the release of serotonin in the brain, like many antidepressants. It also increases the amount of norephinephrine in the brain like some other antidepressants and dopamine, which may be of value to Parkinson’s disease patients. Finally, it increases acetylcholine concentrations in the brain, which enhances memory and intelligence.
Vinpocetine has been the object of over 100 studies all over the world. In one study of patients with cerebral insufficiency, they were asked to remember 10 words on a list. They could only remember 6 out of 10 but after using Vinpocetine they were able to remember all of them.
Studies show that regular use of Vinpocetine improves dizziness, headaches, poor coordination, hearing and eyesight, unstable blood pressure, mood instability, insomnia, vertigo, irritability, nervousness and depression.
Vinpocetine takes about a year of continual use to achieve its maximum effect. Effects are noticeable after 3 to 4 weeks of regular use.

CAUTIONS
It does not interact with other substances so can be used together with them. A one-year study failed to show any toxicity.


“You see, I don’t want to do good things, I want to do great things.” ~Alexander Joseph Luthor

I know Lewd Ferrigno personally.

Phosphatidyl Serine - What is it and is it Safe?
Phosphatidyl Serine (PS) is the major phospholipid in the brain that plays a major role in determining the integrity and fluidity of cell membranes. Low levels of phosphatidyl serine in the brain are associated with impaired mental function and depression.
Phosphatidyl Serine is involved in relaying chemical messages throughout the brain, helping brain cells to store and retrieve information. There is good evidence which shows that PS may help restore brain power. Numerous studies establish that PS consistently benefits memory, learning, concentration and mood. PS can be beneficial for children, too, often helping those who have problems learning and responding to discipline.
No side effects or adverse reactions have been reported with Phosphatidyl Serine.

Huperzine A: Brain Booster
Research in China Shows Benefits in Adolescents As Well As Alzheimer’s Patients
by Will Block
Take acetylcholinesterase - please. It’s one of the more unloved substances in the human body, because it acts as a kind of molecular butcher, cleaving other molecules in half with grim efficiency. But at least it’s highly selective, always seeking and destroying only the acetylcholine molecule, which it splits into acetate and choline. Such specificity is characteristic of all enzymes - proteins that are designed to carry out just one task, through their catalytic activity.
Acetylcholine, as most readers probably know, is a versatile neurotransmitter, a messenger molecule that acts throughout the central and peripheral nervous systems to mediate a host of vital functions, including many related to cognition and memory. It is a molecule devoutly to be desired in ample quantities, not only so we can keep all our marbles, but so they can stay bright and shiny for the endlessly varied game of life.
WHEN GOOD MOLECULES GO BAD, AND VICE VERSA
Why then, did Mother Nature unleash an enzymatic assassin to keep cutting the poor acetylcholine molecules in half? Because - and this is as true of biomolecules as anything else - too much of a good thing is a bad thing (think glucose and diabetes, e.g.). There must always be checks and balances and feedback mechanisms to ensure that there is just enough of what we need, neither too little nor too much. And so there are “good” molecules that we need for optimal health, and “bad” molecules (which aren’t really bad, because they serve a necessary purpose) that keep the good ones from creating havoc through overabundance.
Furthermore, in a chemical analogue to military electronic countermeasures technology, there is a second tier of “good” molecules that serve to jam the actions of the bad ones, when necessary, by inhibiting their ability to perform their assigned functions. One such is huperzine A, an acetylcholinesterase inhibitor - bad for acetylcholinesterase and therefore good for acetylcholine. And, like Chinese boxes, there are yet other molecules that inhibit the inhibitors …
In this cats-and-mice game, there is, as always in living organisms, a delicate balance to be maintained. And, as always, the balance can get skewed as we age, for some reasons that we understand and many more that we don’t. In any case, if acetylcholinesterase gains the upper hand and unduly depletes our stores of acetylcholine, really bad things can happen, such as Alzheimer’s disease - not that there is a clear cause and effect there (few things, including Alzheimer’s, are that simple), but there is a strong correlation that can’t be ignored.
GOOD MOLECULE, HUPERZINE!
Huperzine A (HupA for short), an alkaloid found in the Chinese herb Huperzia serrata, is effective in improving cognitive and memory abilities in humans, including those with Alzheimer’s disease. In China, where HupA is used for treating Alzheimer’s and myasthenia gravis, medical scientists have studied its effects on the mental functions of elderly Alzheimer’s patients.1
In a rigorously designed and controlled experiment, 60 patients aged 52 to 80 with impaired faculties were treated with synthetic HupA (200 micrograms twice daily) or placebo for 60 days. They were evaluated with a huge array of both psychological and physiological tests to determine their mental and physical health before and after the treatment - and, in particular, to determine whether it made any difference if the HupA was administered in the form of capsules or tablets.
Based on four of the most important psychological tests, including memory function, the improvement rates in both groups ranged from 43% to 70%; there was no statistically significant difference between the capsule group and the tablet group.
The researchers also set out to observe the action of HupA on the damaging effects of oxygen free radicals in the patients’ plasma and erythrocytes (red blood cells). Biochemical tests showed significant improvement, although not to the reference values for healthy people in the same age group. The authors speculate that long-term treatment with HupA might be required to optimize the results.
The study also reconfirmed the previously demonstrated safety as well as efficacy of HupA.2,3 The only side effects noted were mild to moderate nausea and insomnia, again with no difference between the capsule and tablet groups.
YOUNGSTERS ALSO BENEFIT FROM HUPERZINE
When a nutrient that improves mental function in the aged does the same in the young, that’s really interesting. And that is what Chinese researchers found, in a study designed to determine the efficacy of HupA on memory and learning in adolescents.4 They selected 34 matched pairs of apparently normal junior middle school students whose only significant complaints were of poor memory and difficulty in learning.
The pairing was done in terms of age, sex, memory quotient, and overall psychological health, to ensure that comparisons would be meaningful. Using these criteria, the researchers found no statistically significant baseline differences between the students in the two groups, one of which was to be treated with HupA, the other to receive a placebo.
In a double-blind trial, one member of each pair, chosen randomly, was given 100 micrograms of synthetic HupA twice daily for four weeks, while the other member received the placebo. The students’ memory quotients were measured before and after the trial, and their academic performance in their Chinese, English, and mathematics lessons was monitored as well.
The results: At the end of the study, the HupA group scored significantly better than the control group on standard memory tests described as “accumulation,” “recognition,” “reproduction,” “association,” “tactual [tactile] memory,” and “number of recitation,” but not on tests of “picture memory” or “understanding.” They had also done significantly better in their Chinese and English lessons, but not in math. No side effects of any kind were noted.
HUPERZINE IS PREFERABLE TO PRESCRIPTION DRUGS
Huperzine A is superior to the drugs tacrine and donepezil, which are acetylcholinesterase inhibitors widely prescribed for Alzheimer’s disease. There is no question that these drugs are effective, but it is our view that chemical compounds derived from natural sources are preferable to those invented by chemists, because the natural ones are typically safer and freer from unwanted side effects.
References
Xu SS, Cai ZY, Qu ZW, Yang RM, Cai YL, Wang GQ, Su XQ, Zhong XS, Cheng RY, Xu WA, Li JX, Feng B. Huperzine-A in capsules and tablets for treating patients with Alzheimer’s disease. Acta Pharmacol Sin 1999 Jun;20(6):486-90.
Xu SS, Guo ZX, Wang Z, Du ZM, Xu WA, Yang JS, et al. Efficacy of tablet huperzine-A on memory, cognition, and behavior in Alzheimer’s disease. Acta Pharmacol Sin 1995;16:391-5.
Xu SS, Xie HB, Du ZM, Tong ZH, Shi QC, Lu KM, et al. Efficacy of tablet huperzine-A on memory and cognition in patients with benign senescent forgetfulness. Chin J Clin Pharmacol Ther 1997;2:1-4.
Sun QQ, Xu SS, Pan JL, Guo HM, Cao WQ. Huperzine-A capsules enhance memory and learning performance in 34 pairs of matched adolescent students. Acta Pharmacol Sin 1999 Jul;20(7):601-3.
Niacinamide is an amine form of niacin and is important in promoting a healthy nervous system, skin, and gastrointestinal functioning. Niacinamide lacks the side effects associated with niacin or nicotinic acid such as flushing. Niacinamide does not have the ability to lower cholesterol.

Thioctic Acid(alpha-Lipoic Acid) is used as Vitamin B family, also a kind of antioxidant. Proved by scientific research . Thioctic has a fairly good effect on improving human’s physique and antigonistic free radical, protecting genetic materials. Slow the speed of senility and prevent diseases such as cardiopathy and cancers. A latest research shows that thioctic acid has obvious effect on the prevention and treatment of diabetes.

DMAE (2-dimethylaminoethanol) is a chemical that has been used to treat a number of conditions affecting the brain and central nervous system. Like other such treatments, it is thought to work by increasing production of the neurotransmitter acetylcholine, although this has not been proven.
Therapeutic Uses
Preliminary evidence suggests that DMAE may be helpful for attention deficit hyperactivity disorder (ADHD).1,2
More widely marketed today as a memory and mood enhancer, DMAE is said to improve intellectual functioning; however, there are no clinical studies that support its use for these purposes. The basis for such claims probably stems from its purported ability to increase levels of a neurotransmitter called acetylcholine. Drugs and supplements called “cholinergics” that increase acetylcholine have been used to treat Alzheimer’s dementia, tardive dyskinesia, and Huntington’s chorea. Because DMAE was believed to be a cholinergic, it has been tried for all of these disorders. However, well-designed placebo-controlled studies have yielded almost entirely negative results.3-9 In addition, there is some controversy over whether DMAE really increases acetylcholine at all.10
What Is the Scientific Evidence for DMAE?
ADHD (Attention Deficit Hyperactivity Disorder)
There is some evidence that DMAE may be helpful for ADHD, according to studies performed in the 1970s. Two such studies were reported in a review article on DMAE.11 Fifty children aged 6 to 12 years who had been diagnosed with hyperkinesia (their diagnosis today would likely be ADHD) participated in a double-blind study comparing DMAE to placebo. The dose was increased from 300 mg daily to 500 mg daily by the third week, and continued for 10 weeks. Evaluations revealed statistically significant test score improvements in the treatment group compared to the placebo group.
Another double-blind study compared DMAE with both methylphenidate (Ritalin) and placebo in 74 children described as having unspecified “learning disabilities” (also probably what we would call ADD today).12 It found significant test score improvement for both treatment groups over a 10-week period. Positive results were also seen in a small open study.13
Alzheimer’s Disease
Most people over the age of 40 experience some memory loss, but Alzheimer’s disease is much more serious, leading to severe mental deterioration (dementia) in the elderly. Microscopic examination shows that in the areas of the brain involved in higher thought processes, nerve cells have died and disappeared, particularly cells that release the chemical acetylcholine. Drugs such as tacrine and danazol, and supplements such as huperzine A, are used for Alzheimer’s based on their ability to increase acetylcholine levels. Because DMAE is also thought to increase acetylcholine, trials have been performed to test its effectiveness for the same purpose. However, there is no real evidence as yet that it works.
A double-blind placebo-controlled study involving 27 patients with Alzheimer’s disease tested DMAE as a treatment.14 Thirteen participants were placed in the group receiving DMAE; however, 6 of them had to drop out of the study because of side effects such as drowsiness, increased confusion, and elevated blood pressure. In those completing the trial, no differences were seen between the treatment group and those taking placebo.
An open trial enrolling 14 patients found no improvement in either memory or cognitive function. The researchers did note improvements in symptoms of depression, but in the absence of a placebo group this observation means little.15
Tardive Dyskinesia
Tardive dyskinesia (TD) is a potentially permanent side effect of drugs used to control schizophrenia. This late-developing (tardy, or tardive) complication consists of annoying, uncontrollable movements (dyskinesias), particularly in the face.
Based on its supposed cholinergic effect, DMAE has been proposed as a treatment for TD. Although some case reports and open studies seemed to suggest that DMAE might be useful for this purpose,16,17 properly designed studies using double-blind methods and placebo control groups have not borne this out. Of 12 double-blind studies reviewed, only one found DMAE to be significantly effective when compared with placebo.18 A meta-analysis of proposed treatments for TD found DMAE to be no more effective than placebo.19 It seems likely, though not entirely certain, that the benefits seen in open studies and individual cases were the result of a placebo effect. However, it is also possible that some particular individuals respond well to DMAE, even if most don’t.
Huntington’s Chorea
Huntington’s chorea is a genetically inherited disease that results in personality changes and, somewhat similarly to TD, uncontrolled spastic movements. It doesn’t usually become symptomatic until a person’s age reaches the late thirties or older, although about 10% of people with Huntington’s will begin to show signs of the disorder in childhood or adolescence.
DMAE was not found to be an effective treatment for Huntington’s chorea in double-blind placebo-controlled trials, although mixed results have been obtained using DMAE in open trials.20,21,22
Safety Issues
Although most clinical investigations using DMAE report that the participants experienced no side effects, enough researchers have found adverse reactions to suggest that some caution is appropriate in using this supplement. One study, as noted above, reported increased confusion, drowsiness, and elevated blood pressure;23 another reports headache and muscle tension as possible adverse effects;24 and another paper suggests that weight loss and insomnia may accompany use of DMAE.25 There is also one case report of a woman who developed severe TD after taking DMAE for 10 years for a hand tremor.26 Besides this, a number of manufacturers warn against the use of DMAE by people with epilepsy or a history of convulsions.
Maximum safe dosages for young children, pregnant or nursing women, or people with severe liver or kidney disease have not been established.
References
1. Re’ O. 2-Dimethylaminoethanol (deanol): a brief review of its clinical efficacy and postulated mechanism of action. Curr Ther Res Clin Exp. 1974;16:1238-1242.
2. Knobel M. Approach to a combined pharmacologic therapy of childhood hyperkinesis. Behav Neuropsychiatry. 1974 Apr-1975 Mar;6:87-90.
3. Casey DE, Denney D. Dimethylaminoethanol in tardive dyskinesia [letter]. N Engl J Med. 1974;291:797.
4. Re’ O. 2-Dimethylaminoethanol (deanol): a brief review of its clinical efficacy and postulated mechanism of action. Curr Ther Res Clin Exp. 1974;16:1238-1242.
5. Alphs L, Davis JM. Noncatecholaminergic treatments of tardive dyskinesia. J Clin Psychopharmacol. 1982;2:380-385.
6. Soares KV, McGrath JJ. The treatment of tardive dyskinesiaa systematic review and meta-analysis. Schizophr Res. 1999;39:1-18.
7. Caraceni TA, Girotti F, Celano I, et al. 2-dimethylaminoethanol (deanol) in Huntington’s chorea. J Neurol Neurosurg Psychiatry. 1978;41:1114-1118.
8. Tarsy D, Bralower M. Deanol acetamidobenzoate treatment in choreiform movement disorders. Arch Neurol. 1977;34:756-758.
9. Fisman M, Mersky H, Helmes E. Double-blind trial of 2-dimethylaminoethanol in Alzheimer’s disease. Am J Psychiaty. 1981;138:970-972.
10. Zahniser NR, Chou D, Hanin I. Is 2-dimthylaminoethanol (deanol) indeed a precursor of brain acetylcholine? A gas chromatographic evaluation. J Pharmacol Exp Ther. 1977;200:545-559.
11. Re’ O. 2-Dimethylaminoethanol (deanol): a brief review of its clinical efficacy and postulated mechanism of action. Curr Ther Res Clin Exp. 1974;16:1238-1242.
12. Re’ O. 2-Dimethylaminoethanol (deanol): a brief review of its clinical efficacy and postulated mechanism of action. Curr Ther Res Clin Exp. 1974;16:1238-1242.
13. Knobel M. Approach to a combined pharmacologic therapy of childhood hyperkinesis. Behav Neuropsychiatry. 1974 Apr-1975 Mar;6:87-90.
14. Fisman M, Mersky H, Helmes E. Double-blind trial of 2-dimethylaminoethanol in Alzheimer’s disease. Am J Psychiaty. 1981;138:970-972.
15. Ferris SH, Sathananthan G, Gershon S, et al. Senile dementia: treatment with Deanol. J Am Geriatr Soc. 1977;25:241-244.
16. Casey DE, Denney D. Dimethylaminoethanol in tardive dyskinesia [letter]. N Engl J Med. 1974;291:797.
17. Re’ O. 2-Dimethylaminoethanol (deanol): a brief review of its clinical efficacy and postulated mechanism of action. Curr Ther Res Clin Exp. 1974;16:1238-1242.
18. Alphs L, Davis JM. Noncatecholaminergic treatments of tardive dyskinesia. J Clin Psychopharmacol. 1982;2:380-385.
19. Soares KV, McGrath JJ. The treatment of tardive dyskinesiaa systematic review and meta-analysis. Schizophr Res. 1999;39:1-18.
20. Caraceni TA, Girotti F, Celano I, et al. 2-dimethylaminoethanol (deanol) in Huntington’s chorea. J Neurol Neurosurg Psychiatry. 1978;41:1114-1118.
21. Tarsy D, Bralower M. Deanol acetamidobenzoate treatment in choreiform movement disorders. Arch Neurol. 1977;34:756-758.
22. Re’ O. 2-Dimethylaminoethanol (deanol): a brief review of its clinical efficacy and postulated mechanism of action. Curr Ther Res Clin Exp. 1974;16:1238-1242.
23. Fisman M, Mersky H, Helmes E. Double-blind trial of 2-dimethylaminoethanol in Alzheimer’s disease. Am J Psychiaty. 1981;138:970-972.
24. Haug BA, Holzgraefe M. Orofacial and respiratory tardive dyskinesia: potential side effects of 2-dimethylaminoethanol (deanol). Eur Neurol. 1991;31:423-425.
25. Sergio W. Use of DMAE (2-dimethylaminoethanol) in the induction of lucid dreams. Med Hypothesis. 1988;26:255-257.
26. Haug BA, Holzgraefe M. Orofacial and respiratory tardive dyskinesia: potential side effects of 2-dimethylaminoethanol (deanol). Eur Neurol. 1991;31:423-425.


“You see, I don’t want to do good things, I want to do great things.” ~Alexander Joseph Luthor

I know Lewd Ferrigno personally.

Basically you have a Mc Donald’s Style packaging of smart drugs in one compound. Almost all this shit is in individual entries in my nootropics thread.


“You see, I don’t want to do good things, I want to do great things.” ~Alexander Joseph Luthor

I know Lewd Ferrigno personally.

Damn, Twatt, you’re amazing! BodyQuicken sounds like it has the potential to be OK.

Thanks for the write-up.

Now, I’ve seen phosphatidyl serine recommended for control of cortisol to keep it from cannibalizing muscle tissue. Did you see anything about that in your sources?

T3


Tex3

"Sadly, however, seconds after its launch, it undergoes SMEF, or Spontaneous Massive Existence Failure,and disappears." Douglas Adams

Tex did you buy this stuff yet? I think I saw this a few months ago in a Martial Arts Magazine. It was advertised to improve hitting or reaction speeds.


“You see, I don’t want to do good things, I want to do great things.” ~Alexander Joseph Luthor

I know Lewd Ferrigno personally.

Quote
Originally posted by twatteaser
Tex did you buy this stuff yet? I think I saw this a few months ago in a Martial Arts Magazine. It was advertised to improve hitting or reaction speeds.

No. The price made me think for a change, something like:
1. I’m already taking PS and DMAE in abundant amounts.
2. Niacinamide is easy to come by if it’s not already in my multiple and stress B supplements.
3. Huperzine and Vinpocetine I want to try and can buy them separately.

The articles you provided woke me up even further, like:
1. One needs 800 mg of active PS to get the cortisol lowering effect, but one must take 4000mg of PS to get 800 mg of active PS. (AST-SS) This is too expensive.
2. When one takes PS, the digestive process breaks it down to its components - glycerol, fatty acids, and phosphorylated serine. When PS is needed, the body assembles it from phosphorylated serine and whatever fatty acids are handy, so there doesn’t seem to be any advantage to taking PS since it’s broken down and reassembled from other ingredients. Taking phosphorylated serine alone stimulates production of PS. (Dr. Debe)

And it does seem to be cheaper.

The only internet source I’ve found so far is http://lifeextensionvitamins.com/serphosser.html

They show a related item named Holy Basil, an ayurvedic botanical that also lowers cortisol, but
that’s a whole ‘nother study.

T3


Tex3

"Sadly, however, seconds after its launch, it undergoes SMEF, or Spontaneous Massive Existence Failure,and disappears." Douglas Adams

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