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PIRACETAM DOSAGE - Why you should be taking 4.8 grams / dose

piracetam racetam memory nootropic cognitive cognition learning pramiracetam oxiracetam aniracetam

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#151 xsiv1

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Posted 11 July 2013 - 08:56 PM

I've personally experimented with 10 gram doses per day and for an extended period without any discernible difference from 1600mgs per dose X 2 per day. Guess I don't respond to piracetam like the other racetams and Noopept which at a mere 10mgs with some Krill oil is more effective than the various brands of piracetam I've used. I know piracetam is working, but higher doses don't do anything significantly different than lower doses... for me anyways. :blink:
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#152 SlimNm

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Posted 28 July 2013 - 02:05 PM

Hi, Cerebral Health!

I've read some bad reviews about your site, but I think that the positive ones outweigh them. I'm going to find out soon ;)

Just wanting to know how my order #248391596795896 is doing, and when is the estimated arrival date?

Thanks so much! You can send me a private message on this forum requesting my phone number if you want to speak to me personally.

I would email you, but it seems that your email, synapse@cerebralhealth.com is no longer a valid email.

I will be sure to leave you positive reviews on a couple forums, including this one, and on reddit.com, if I get my shipment in soon xD

Edited by SlimNm, 28 July 2013 - 02:05 PM.

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#153 SlimNm

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Posted 28 July 2013 - 11:28 PM

Bump. Paging CerebralHealth, come in. Do you copy? Over.
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#154 Brundle99

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Posted 29 July 2013 - 12:30 AM

I have bought Piracetam from Cerebral Health a few times before, and they seemed to be a well established nootropics supplier, but not that long ago there was an FDA report that said CH had not labeled some products, and they were given a warning to rectify this.

They are more expensive than many other suppliers, but when you think your buying quality, it isn't an issue to spend a bit more.

The problem now seems that CerebralHealth......(the username of a guy on here) who I think either runs, or is a part of the Company, has gone from not reponding to messages very often... to not at all.

Don't think the email address from CH is even valid anymore.

He used to be quick to defend the Company when people labeled it a scam and what not, but iy doesn't aspire much confidence for a customer.

I don't think I will be using them again.

Edited by Brundle99, 29 July 2013 - 12:32 AM.


#155 xsiv1

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Posted 29 July 2013 - 02:29 AM

I've also read, although unsure if confirmed, that some of their products were not of the proper potency, or were swapped with another product. I've never used them so don't have any experiences to share except for the faint memory of what I've read. It's not good that they're not responding to any of your communications. I considered using them once until I read that part about their product. I think it was on Reddit Slim

#156 Brundle99

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Posted 29 July 2013 - 09:34 AM

A bit worrying really, the least you would expect is that your ingesting the product you paid for and not something else.

I think the Piracetam I bought from them is ok although not sure about potency, it says 99% on the bag but who knows. It is crystalline white powder similar consistency to sugar, which is what it's supposed to look like from research.

I've only ever had subtle effects from the rides I've tried from 800-4.8 in the past, so could be I just haven't found my idea dose, I hope it's not a question of potency anyway.

I've just bough Centrophenoxine from a different supplier, does anyone have good experiences with that combo?.

I wish there was a way to tell what your getting, because powder could be anything....

I'm going to try and get something on prescription as I have memory problems and I'm only 31.

#157 8bitmore

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Posted 29 July 2013 - 09:47 AM

A bit worrying really, the least you would expect is that your ingesting the product you paid for and not something else.

I think the Piracetam I bought from them is ok although not sure about potency, it says 99% on the bag but who knows. It is crystalline white powder similar consistency to sugar, which is what it's supposed to look like from research.

I've only ever had subtle effects from the rides I've tried from 800-4.8 in the past, so could be I just haven't found my idea dose, I hope it's not a question of potency anyway.

I've just bough Centrophenoxine from a different supplier, does anyone have good experiences with that combo?.

I wish there was a way to tell what your getting, because powder could be anything....

I'm going to try and get something on prescription as I have memory problems and I'm only 31.


If you search for doc simon then you'll find online vendor that sells Piracetam tablets made by Merck and other big pharmas if you feel more comfortable with that (price almost same gram for gram if you order a few packages at the same time, I have ordered several times without no hiccups beyond a bit of wait (around 10days and that's from one EU country to another)) - there's is no easy/cheap way to validate no-name powders. I would seriously consider adding cod-liver oil at about 5-10ml a day in order to get big dose of DHA/EPA along with vitamin a/d - for me this is, even by itself, a stronger/more "felt" medicine as compared to Piracetam.

#158 Brundle99

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Posted 29 July 2013 - 10:23 AM

I started taking fish oil capsules and got the COA to verify it, it wasn't rancid anyway. I think maybe I felt a bit more of Piracetam when I did take it at 3-4g a day, but since ran out.

I also take a centrum multivitamin with Piracetam.

I was a little worried about all these things adding to too much blood thinning though.

Some people say add MSG and calcium too but I don't know.

I still have three quarters of the 1k bag from CH so may try adjusting dose or adding FO again.

I have a thyroid condition which I have heard this may affect my response with Piracetam. Hope not!.

I've been try Piracetam on and off since December and didn't get on well with the choline bitartrate but Centrophenoxine makes you feel a bit more energetic and will be more bioavailabile and top quality.

I welcome any comments!

#159 Sunwind

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Posted 29 July 2013 - 03:08 PM

Seriously guys can you not take this to another topic? what does this specific supplier have to do with the original post? I came here hoping to see a few more replies about 4.8g+ Pira dosing and all I see is this nonesense. Does this forum even have moderators?
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#160 Brundle99

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Posted 29 July 2013 - 05:33 PM

Seeing as this is pretty much a dormant thread and discussion is still about Piractem doses and what not, I wouldn't have thought it would be an issue. If anyone has any new information on the 4.8g then feel free.

It's not nonsense in any way, everyone is trying to help each other out, and that's the purpose of this is it not??.
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#161 deh707

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Posted 29 July 2013 - 06:50 PM

Personally, the higher the Piracetam dose, the more it makes me quite irritable and sleepy.

I've recently tried 4.8g and it was no different; probably worse than how 2.4g affects me.

Seems I require much smaller doses, such as a mere 400-450mg.

#162 Brundle99

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Posted 29 July 2013 - 07:13 PM

I have tried up to 5g for a few weeks and it didn't change my response to Piracetam, but we all know its dose dependant and it varies greatly from person to person.

The fish oil a lot of people agree its synergistic with Piracetam but can't say I tried it long enough to really see the effects.

I have read in forums that some people respond to doses as low as 300mg, I'm going to start again at 500mg and change up every 2 weeks by 250mg until I notice things. Probably wont go any higher than 9.6g if it gets that high.



#163 xsiv1

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Posted 29 July 2013 - 07:32 PM

I've tried doses at high levels, modest levels and lower levels and found that about 1600mgs-2200mgs is about right for me. Normally I'll only take a capsule of 300mgs Alpha-GPC with it but I do take fish oils in the morning. I just didn't see any benefit to taking high doses especially when weighing it against cost.

Edited by xsiv1, 29 July 2013 - 07:33 PM.


#164 Brundle99

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Posted 29 July 2013 - 07:50 PM

Yeah I don't like the idea of taking high doses of Piracetam, even if there's no established LD50.

If the response is 2.2 then a 1g bag will last ages.

Never tried with Alpha GPC but only because I'm hypothyroid and AGPC is highly refined Soy Lecithin, which will probably make my symptoms worse.

There's also a forum on here about high dose fish oil with Piracetam that's interesting, and people swear by it.

#165 Razor444

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Posted 26 February 2014 - 10:10 AM

Recently took a trip to Macao and decided to grab up a box of Nootropil from a local pharmacy. Cost was approximately $6USD for 90 x 800mg tablets.

I found it interesting that the recommended dosage was in fact 4.8g per day for the first few weeks. But it's suggested to drop down to a maintenance dose of 2.4g per day after that.

I found it more interesting that after 4 days of taking ~4.8g per day I was actually noticing effects from piracetam. This is after accepting defeat and thinking it was totally ineffective for me personally since I've done 3-4 week trials of diligently dosing powder each day with absolutely zero effects on cognition.

I looked at the ingredients on these tablets and there seems to be a lot of mannitol. I'm guessing the mannitol is improving delivery of the piracetam in the tablets across the blood brain barrier. So since I've still got almost a full kilo of piracetam I ordered up some mannitol from ebay and made a solution of piracetam + mannitol. I reduced it to a solid form and ground it up again.

So I've got about 100g of piracetam and mannitol mix that I plan on doing a trial with here in the next couple of days to see if mannitol is the key to piracetam efficacy for me personally. Will update when I get a chance. Attached is a scan of the insert provided with the Nootropil I bought.



What's your current dosage, manic_racetam? Did you continue with the suggestion of 4.8g per day for the first few weeks, and 2.4g thereafter?

#166 hackitall

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Posted 27 March 2014 - 09:52 AM

Hi all,

Complete noob here, so please forgive me if I say something off. I got to this forum in the last few days while searching for more information on piracetam. I recently purchased nootropil 800 (piracetam 0.8 gm). Took my first pill yesterday evening and it kicked in within an hour with the effects lasting upto 5 hours. I feel as though 4.8 grams maybe way too high for me. A little background, I have no issues as such but am trying to use paracetamol for the heightened clarity and ability to focus. What I am looking for is help with dosage amounts and some guidelines for long term use.

I really appreciate the help and sorry again if I made a mistake in my post.

Thanks.

#167 Joe Cohen

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Posted 03 May 2014 - 12:08 AM

I think anything over 800mg is too high.  Piracetam causes oxidative stress in the hypothalamus.   

MDA[a marker for oxidative stress]…. increased in cortex and hippocampus and in cortex, hypothalamus and striatum by the higher dose of vinpocetine or piracetam, respectively along with decreased TAC (total antioxidant capacity)….at their high concentration, these drugs exhibit pro-oxidant properties and increase free radical production or act as a free radical….[Ref.]

The high dosage that this study refers to is 300mg/kg.

For somebody who weighs an average weight of 68kg, this would be equivalent to 20.4g, but when converted to an equivalent human dosage, it would be 3.25g.

http://selfhacked.co...with-piracetam/


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#168 Metagene

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Posted 03 May 2014 - 01:53 AM

Cohen I think you missed the point of that study:

We studied the role of oxidative stress and the effect of vinpocetine (1.5, 3 or 6 mg/kg) and piracetam (150 or 300 mg/kg) in acute demyelination of the rat brain following intracerebral injection of ethidium bromide...


Edited by Metagene, 03 May 2014 - 01:54 AM.

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#169 Joe Cohen

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Posted 03 May 2014 - 03:01 AM

But "high" doses of  piracetam made these effects worse. Why is that?



#170 Metagene

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Posted 03 May 2014 - 04:16 AM

But "high" doses of  piracetam made these effects worse. Why is that?


If you look at the study again it merely states after a intracerebral injection of ethidium bromide high doses of piracetam and vinpocetine increased malondialdehyde (a marker for oxidative stress) but in turn increased gutothioine and lowered serum nitric oxide. This does not imply piracetam alone increases oxidative stress.

Edited by Metagene, 03 May 2014 - 04:20 AM.

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#171 Metagene

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Posted 03 May 2014 - 04:28 AM

I don't have full access to other studied linked on your site you should look at this too: http://www.ncbi.nlm....pubmed/7301036/

Although choline administration raised choline content about 50% in striatum and cortex, changes in acetylcholine levels were much more subtle (only 6-10%). No significant changes following choline administration were observed in the hippocampus. However, piracetam alone markedly increased choline content in hippocampus (88%) and tended to decrease acetylcholine levels (19%).


Edited by Metagene, 03 May 2014 - 04:32 AM.

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#172 Joe Cohen

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Posted 03 May 2014 - 04:51 AM

Why would piracetam only increase OS when ethidium bromide is also added?  

 

EB is irrelevant.  The point is piracetam increases OS in the hypothalamus in an animal model of acute demyelination.  I don't see why this wouldn't be the case in normal animals.

 

Please clarify your point with the last post.


Edited by Joe Cohen, 03 May 2014 - 04:55 AM.

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#173 Metagene

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Posted 03 May 2014 - 12:29 PM

No It never said piracetam directly increased oxidative stress only it's marker MDA. The high doses of piracetam lead to an increase of gutothioine and lowered nitric oxide which would oppose oxidative stress. I realize this a oversimplification but notice EB caused an increase of MDA then lowered gutothioine and increased nitric oxide.

Edited by Metagene, 03 May 2014 - 12:33 PM.

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#174 Joe Cohen

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Posted 03 May 2014 - 03:14 PM

And why isn't its marker MDA a good indicator?  Yes, it increased glutathione A LITTLE, which makes the situation a bit better, but total antioxidative capacity decreased.

 

The measure of antioxidant capacity (AC) considers the cumulative action of all the antioxidants present in plasma and body fluids, thus providing an integrated parameter rather than the simple sum of measurable antioxidants. The capacity of known and unknown antioxidants and their synergistic interaction is therefore assessed, thus giving an insight into the delicate balance in vivo between oxidants and antioxidants. Measuring plasma AC may help in the evaluation of physiological, environmental, and nutritional factors of the redox status in humans. Determining plasma AC may help to identify conditions affecting oxidative status in vivo (e.g., exposure to reactive oxygen species and antioxidant supplementation). 

http://www.ncbi.nlm....pubmed/11121717

 

I decided to look at the full study because the abstract isn't completely clear.

 

MDA increases with piracetam over ethidium control.  High dosage piracetam increased MDA the most out of all the groups.

Malondialdehyde is generated from reactive oxygen species (ROS), and as such is assayed in vivo as a bio-marker of oxidative stress.[3]

https://docs.google....it?usp=drivesdk

 

 

TOTAL ANTIOXIDANT CAPACITY decreases with piracetam in both dosages (statistically significant), but not really vinpocetine (never had an issue with vinpocetine).  Strangely, TAC went up a little in the higher dosage, but was still significantly lower.  My guess is at a certain level of OS, GSH/other endogenous antioxidants production ramped up and combated the OS, but reduced glutathione glutathione isn't an unlimited resource.   But still, piracetam likely contribute to OS burden by increasing MDA and possibly other oxidants.

https://docs.google....it?usp=drivesdk

 

Glutathione increases with the higher dosages of piracetam.  But, again, chronic usage doesn't appear to be wise given that glutathione isn't an unlimited resource.  Combine sleep deprivation, toxins, etc..and you get too much of an OS burden...

https://docs.google....it?usp=drivesdk

 

"In case of piracetam, the

highest dose of the drug increased lipid peroxidation in
brain, whilst eliciting increased brain GSH. An intriguing
explanation for these observations is that at their high
concentration, these drugs exhibit pro-oxidant properties
and increase free radical production or act as a free radical
and in this latter case, it is possible that either piratcetam or
vinpocetine react with other free radicals or antioxidant
systems other than glutathione, which is spared in this
condition."

 

I think the author sums up the findings well in their discussion.

 

"In summary, findings in the present study indicates that
demyelination due to the local injection of ethidium bromide
into the rat brain is associated with increased oxidative
stress. The study suggests an antioxidant effect for the
nootropic drugs vinpocetine and piracetam at low doses. In
contrast, the higher doses were associated with an increase
in oxidative stress, though both drugs offered significant
protection against GSH depletion induced by ethidium
bromide. The clinical significance of these findings needs
to be determined."
 
If I only saw these studies, I would be skeptical.  But piracetam's common side effects of brain fog suggest that oxidative stress in the hypothalamus is actually happening in people.  The longer people take it the more likely they will experience brain fog, especially when combined with other stressor.
 
Interestingly, it could be from increased dopamine production:
 
"Piracetam has been reported to increase dopamine in
cortics and striatium [56–58] which might increase free
radical production. Dopamine is subject to auto-oxidation
to semiquinone and quinones generating free radicals such
as superoxide anion, peroxynitrite, hydroxyl radical and
nitrate radical. Semiquinones and quinines themselves can
form conjugates with thiol compounds such as GSH and
L-cysteine, and generate other radicals that are also toxic
[59]. It is therefore possible that at high doses, both vinpocetine
and piracetam might increase free radical production
through their effect on dopamine level in brain."
 

Edited by Joe Cohen, 03 May 2014 - 04:01 PM.

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#175 Metagene

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Posted 03 May 2014 - 03:38 PM

I know you have good intentions Joe. Just don't fall victim to confirmation bias by ignoring the larger context. This should help clarify things a bit.

Demyelinating diseases of the central nervous system are a heterogeneous group of chronic inflammatory disorders, the hallmark of which is loss of myelin sheath and nerve conduction deficits leading to motor and/or sensory dysfunction and are the leading cause
of nontraumatic neurological disability in young adults (Hu and Lucchinetti, 2009). The spectrum of demyelinating disorders includes 'autoimmune' inflammatory demyelinating diseases, the inflammatory demyelinating diseases of infectious aetiology, and the de- myelinating or dysmyelinating diseases of genetic/hereditary background. In addition, primary demyelination is present in other conditions, such as brain ischaemia and in- toxication (Lassmann, 2001). Multiple scle- rosis is by far the most common inflammato- ry demyelinating disease leading to focal plaques of primary demyelination with a var- iable degree of axonal and neuronal degener- ation (Love, 2006; Lassmann et al., 2007).
Oxidative stress has been implicated in both normal aging and in various neuro- degenerative disorders. In the brain, the high content of polyunsaturated fatty acids, the high utilization of oxygen account for the susceptibility to free radical damage. The mechanisms of tissue injury in demyelinating diseases of the central nervous system are poorly understood but increasing evidence support a role for oxidative stress due to an imbalance between free radicals generation and endogenous antioxidant mechanisms. Reactive oxygen species, nitric oxide, and proinflammatory cytokines released by mon- ocyte-derived macrophages contribute to neu- roinflammation, demyelination and axonal damage and disease progression in multiple sclerosis (Mirshafiey and Mohsenzadegan, 2009; Smith, 2011; de Vries et al., 2011).


Multiple sclerosis patients showed increased generation of superoxide free radicals in blood (Glabinski et al., 1993), elevated levels of thiobarbituric acid reactive substances and reduced protein sulfhydryl groups in cerebro- spinal fluid and serum (Mitosek-Szewczyk et al., 2010), suggesting increased free radical production and lipid peroxidation. Oxidized lipids and DNA were highly enriched in ac- tive multiple sclerosis plaques (Haider et al., 2011). Evidence also implicates increased nitric oxide generated by the inducible form of nitric oxide synthase (iNOS) in the in- flammation and demyelination in multiple sclerosis. Increased iNOS activity has been demonstrated in monocytes/macrophages and/or astrocytes in demyelinating lesions of postmortem tissues in multiple sclerosis (Ba- gasra et al., 1995; Oleszak et al., 1998; Liu et
al., 2001). Nitric oxide is increased in serum of patients with multiple sclerosis (Ibragic et al., 2012). Nitric oxide is likely to be in- volved in axonal and neuronal injury in de- myelinating conditions (Kapoor et al., 2000; Garthwaite et al., 2002).


Nitric oxide is an important molecule in- volved in synaptic transmission and regula- tion of vascular tone. Nitric oxide is produced within the central nervous system from L- arginine by a constitutive (neuronal) form of nitric oxide synthase (nNOS), an endothelial form in vascular endothelium (eNOS) or an inducible form (iNOS) localized to glia, and requires activation by endotoxin and cyto- kines (Moncada and Bolaños, 2006). The production of nitric oxide is increased in brain and serum of multiple sclerosis patients (De Groot et al., 1997; Liu et al., 2001; Koch et al., 2008). Nitric oxide is a free radical and can react with many other free radicals e.g., superoxide radical generating peroxynitrite radical, capable of causing oxidative changes to macromolecules e.g., proteins, lipids and DNA (Moncada and Bolaños, 2006). Elevated nitric oxide concentrations which occur in neuroinflammatory states can thus result in neurodegeneration. Increased levels of nitric oxide causes axonal degenera- tion (Kapoor et al., 2000; Garthwaite et al., 2002) and activation of nNOS in oligoden- drocytes leads to oligodendrocyte injury re- sulting in demyelination (Yao et al., 2010). Evidence also implicates iNOS in the in- flammation and demyelination of optic neuri- tis, where localized loss of myelin proteins, myelin breakdown, and the presence of iNOS and nitrotyrosine were associated with in- flammatory infiltrates on the edges of the nerve and reactive astrocytes (Tsoi et al., 2006).


http://www.excli.de/...32012_proof.pdf

#176 Joe Cohen

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Posted 03 May 2014 - 03:55 PM

Metagene,

You mean well, but don't fall prey to your apriori belief that piracetam can't have side effects.

 

Your response doesn't address any of my points.  As a result, I will end the discussion here.

 

Be well,

Joe

 


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#177 Metagene

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Posted 03 May 2014 - 04:55 PM

*Sigh*

When exactly did I say I believe piracetam was side effect free? FYI I followed up my own response prior to reading your post. In any case the information sited does very little to support your theory that brain fog and drowsiness caused by piracetam is a result of increased oxidative stress in the hypothalamus and that's all.


Oxidative stress has been implicated in both normal aging and in various neuro- degenerative disorders.


Edited by Metagene, 03 May 2014 - 05:08 PM.

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#178 Metagene

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Posted 03 May 2014 - 11:42 PM

Interesting enough here is a case report of a 29 year old woman diagnosed with postpartum hypothalamic dysfunction who was given 4.8 grams of piracetam a day that "partially improved the patients general feeling and reduced intensity of complaints. " http://www.endokryno...&indeks_art=513

#179 ChaiWong

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Posted 04 May 2014 - 04:41 AM

I can't post a link since I am a new member but does the study "Analgesic activity of piracetam: Effect on cytokine production and oxidative stress" (available at sciencedirect.com) offer anything relevant to either of your arguments?



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#180 Metagene

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Posted 04 May 2014 - 12:25 PM

The only fact Joe Cohen has established is that at high doses of Piracetam may "exhibit pro-oxidant propertiesand increase free radical production or act as a free radicals" nothing more.Concentration dependent antioxidant/pro-oxidant activity of curcumin studies from AAPH induced hemolysis of RBCs.<a class='bbc_url' href='http://www.ncbi.nlm.nih.gov/m/pubmed/18571152/'>http://www.ncbi.nlm.nih.gov/m/pubmed/18571152/</a>Nicotine's oxidative and antioxidant properties in CNS.<a class='bbc_url' href='http://www.ncbi.nlm.nih.gov/m/pubmed/12377264/'>http://www.ncbi.nlm.nih.gov/m/pubmed/12377264/</a>Resveratrol as an antioxidant and pro-oxidant agent: mechanisms and clinical implications<a class='bbc_url' href='http://www.ncbi.nlm.nih.gov/m/pubmed/17956300/'>http://www.ncbi.nlm.nih.gov/m/pubmed/17956300/</a>The antioxidant and pro-oxidant activities of green tea polyphenols: a role in cancer prevention.<a class='bbc_url' href='http://www.ncbi.nlm.nih.gov/m/pubmed/20558130/?i=2&from=/21538850/related'>http://www.ncbi.nlm.nih.gov/m/pubmed/20558130/?i=2&from=/21538850/related</a>Maybe it's time to beat on a different drum.

Edited by Metagene, 04 May 2014 - 01:16 PM.






Also tagged with one or more of these keywords: piracetam, racetam, memory, nootropic, cognitive, cognition, learning, pramiracetam, oxiracetam, aniracetam

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