piracetam quality lacking

6.9: web.wealth/piracetam:

. I've had many leary perceptions of the racetams
as others said their effects were too subtle
to risk spending much money on .
. but I'm very impressed from today's research
that they cleared aging spots in the brain
(levels of lipofuscin in the rat brain).
. I was concerned that the FDA doesn't allow
sale of Piracetam in the US as a dietary supplement;
I think that means there is no reason to sell you
USP or Food Grade quality;
everyone can save $hundreds on technical grade,
but what are the contaminant levels?
for instance, my contact for high-grade stuff is
they'll sell me anything spectrumchemical makes;
but again, when I check spectrum's site,
the EP* grade requires regulatory approval .
europe's equivalent to our verified food grade .]
. the grade being sold on the street is this .

High dose piracetam therapy to renew NMDA receptors:
. causes anx and suicidal ideation in some;
others find them enormously helpful with ADHD
(especially pramiracetam)
and if anything, exert an antidepressant effect .
. run piracetam for 28 days at doses between
3200-4800mg/day [loses effectiveness if not cycled .]
. the weak racetam drug piracetam
I found to be a useful nootropic
with a mild mood-elevating effect;
the stronger aniracetam and oxiracetam
I found made me anxious but still had a nootropic effect,
while the even stronger again pramiracetam
made me instantly irritable
with a tendency towards depressive thoughts...
maybe individual preference for these drugs
depends on your natural level of NMDA activity.
Effects of Piracetam on NMDA Receptor
Subchronic treatment of aged mice with piracetam
(500 mg/kg p.o. for 14 days)
elevates N-methyl-D-aspartate (NMDA) receptor density
by about 20%
and normalizes the enhanced affinity of
L-glutamate for the NMDA receptor.
Since deficits at the level of the NMDA receptor
might be one of the mechanisms underlying
age-associated cognitive impairment,
the effects reported for piracetam
may be relevant to its cognition-enhancing properties .
Piracetam and other structurally related nootropics.
This review covers literature from 1965 through 1992
of piracetam, oxiracetam, pramiracetam, etiracetam,
nefiracetam, aniracetam rolziracetam
and their structural analogues.
The piracetam-like nootropics are capable of achieving
reversal of amnesia induced by, e.g., scopolamine, ...
No affinity has been found for these receptors:
alpha 1-, alpha 2-, beta-, muscarinic,
5-hydroxytryptamine-, dopamine, adenosine-A1-, mu-opiate,
GABA (except for nefiracetam (GABAA)),
benzodiazepine and glutamate .
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.
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.
Indian Journal of Pharmacology 2002; 34: 439-440

There is a serious decline in acetylcholine receptors
in normal aging in humans.
Piracetam elevates the density of frontal cortex
acetylcholine receptors by 30-40%
restoring the levels of acetylcholine in the brain.
Energy (ATP) is critical to the brain's very survival
and brain cells must produce all their own ATP
from glucose (sugar) and oxygen.
They cannot borrow ATP from other cells.
Brain carbohydrate metabolism is impaired
in a variety of dementias
and the degree of reduction in
brain carbohydrate metabolism
correlated with the severity of the dementia.
Piracetam increases the activity of
adenylate kinase enzyme
that converts ADP into ATP and AMP.
This reduces the drop in ATP in oxygen-compromised brain.
Thus, it prevents the dementia and speeds up the
recovery from hypoxia due to
enhancement of oxidative glycolysis.
It increases cerebral blood flow,
cerebral oxygen usage metabolic rate
and cerebral glucose metabolic rate
in chronic impaired human brain function
i.e., multi-infarct (stroke) dementia,
senile dementia of the Alzheimer type
and pseudo dementia, ischaemic cerebral infarcts .
Piracetam, Alpha-GPC and Choline (and other racetams)
are known to activate cholinergic system
and alleviate cognitive symptoms caused by
extended use of anticholinergic drugs.
not affecting NMDA receptors
It may have an ability to increase enzyme activity
and energy production in intrasynaptic neuron mitochondria[6]
and increased brain oxygen[7] and glucose consumption.[8]
These effects may merely be downstream effects of Piracetam
on ion channels and/or ion transporters[1]
which, by positively modulating AMPA-glutamate receptors,
can increase calcium influx into neurons
and increase the density of AMPA receptor binding sites.[9]
This mechanism of action is similar to Aniracetam and Oxiracetam[9]
and like those two, Piracetam does not significantly affect
the other two glutamate receptor subtypes,
NMDA and Kainate receptors.[9][1]
Piracetam appears to bind to Glu2 and Glu3 subunits of AMPA receptors,
of which Aniracetam binds to Glu3 mostly;
binding to Glu2 is a unique site for Piracetam.[10]
good to know NMDA receptors not over-stimulated:
Glutamate is the main excitatory neurotransmitter
in the mammalian central nervous system (CNS)
and mediates neurotransmission across
most excitatory synapses.4
It binds to three receptors, with glutamate toxicity
apparently being primarily mediated via
glutamate binding to the NMDA glutamate receptor.
NMDA receptors are abundant,
ubiquitously distributed throughout the brain,
fundamental to excitatory neurotransmission,
and critical for normal function.4
    Excess glutamate
chronically over stimulates NMDA receptors
with subsequent release of excess intracellular calcium
leading to neuronal cell death.5, 7, 8, 9
This then causes 'excitotoxicity', that is,
toxicity due to excess stimulation by an excitatory amino acid.
CNS disorders in which glutamate-induced excitotoxicity
are implicated
include cerebral ischaemia, in stroke or brain trauma;
neurodegenerative disorders such as
Parkinson's and Huntington's diseases
and disorders such as epilepsy and neuropathic pain,
in which there is overactivity of excitatory pathways.4, 7
The rationale for the acute treatment of brain ischaemia
with NMDA antagonists is strong10
as nonselective NMDA antagonists are the most
consistently neuroprotective agents
in animal models with stroke.
Nevertheless, clinical trials in stroke and traumatic brain injury
with NMDA antagonists have so far been disappointing.10, 11, 12
Rolipram suppressing Th1 autoimmunity
. some good reviews of a source of pramiracetam: