271 replies to this topic

[unbeatableking]

^

I know that. All of my orders are from SP.

It helps to be a little suspicious once in a while however - especially when your money and health are at stake.

[gizmobrain]

I agree, just throwing that out there in case you didn't know.

[dear mrclock]

with experience i know some companies can be more reliable compared to others on one product and completely fail with entirely different one. so dont just speculate because you got supplement from a company and it worked, their future or entirely different products are as high quality.

i guess only safe way is, someone not associated with the company to review the given supplement and tell us results.

Edited by dear mrclock, 23 August 2012 - 02:30 AM.

[unbeatableking]

^

That is precisely my point.

IMO it sounds suspicious. This d-serine supplement just came out of the blue among their offerings. I was under the assumption that PA was one of the only synthesizers in this country.

Although I wouldn't be surprised. They regularly sift through these forums, looking for the next 'big thing' to sell.

Apart from that? Mccandles has a lot of connections. He must know of a lot of chemical labs. He's been in the business for more than a decade now.

Edited by unbeatableking, 23 August 2012 - 04:13 AM.

[gizmobrain]

It's all about marketing. D-serine has been around for years, but no one was interested in buying it until someone in the states started hyping it. Its not hard to synth.

[Psionic]

I wonder how synergetic can be combo composed off Sarcosine & D-Serine + D-Aspartic Acid with pregnenolone, isnt it too much in one dose?

[gbpackers]

smartpowders made it 29.99.. price dropped on prototype nutrition to them same thing now lol.. i think it's safe to assume given both their reputations that both of them sell legit products. One might've been just trying to take advantage market conditions before.

[dear mrclock]

I wonder how synergetic can be combo composed off Sarcosine & D-Serine + D-Aspartic Acid with pregnenolone, isnt it too much in one dose?

whats with the pregnenolone ? i have tried it, still have it and it does nothing for me. what is it supposed to do anyway ?

[unbeatableking]

smartpowders made it 29.99.. price dropped on prototype nutrition to them same thing now lol.. i think it's safe to assume given both their reputations that both of them sell legit products. One might've been just trying to take advantage market conditions before.

I've been around these circles long enough to know that not all of SP's products are legitimate.

Certain anecdotes online should clue you in.

[Galantamine]

I've had good experiences in the past with Smart Powders, and the D-Serine lab reports appear legitimate, although the N-acetyl-tyrosine they are selling feels completely bunk.

[SuperjackDid_]

How D-Serine strong compare to Monosodium Glutamate to synergistic with Piracetam ?

Monosodium Glutamate is great for very tiny dose ,fast and effective ? i not yet sure ,so need to try this one might safer .

[Galantamine]

How D-Serine strong compare to Monosodium Glutamate to synergistic with Piracetam ?

Monosodium Glutamate is great for very tiny dose ,fast and effective ? i not yet sure ,so need to try this one might safer .

Monosodium glutamate is a salt of glutmate and will dissociate into its parent ions upon ingestion. Needless to say, glutamate has very poor blood brain barrier penetration, and is effectively effluxed to maintain a very narrow concentration range. This is why D-Aspartic acid, sarcosine, and now D-Serine, are novel. Dietary glutamate also undergoes significant periperhal conversion, and so would be inefficient even with increased BBB penetration.

[unbeatableking]

People are thinking of combining sarcosine with d-serine. What do you think? Upvoted btw.

[metaprog]

My primary interest is in combing D-Serine with D-Aspartic Acid. From what IrishMD's blog & the web has elucidated, activating the co-agonist sites (DAA at the glutamate & D-Serine @ the glycine) together should hopefully provide a potent synergistic effect.

Has anyone taken D-Serine yet?? It would be great if anyone with experience taking D-Serine would share his/her experience.

[ScienceGuy]

Please kindly note that anyone suffering from or recovering from LYME DISEASE (BORRELIOSIS) and its associated CO-INFECTIONS should avoid D-SERINE, as well as any and all other NMDA RECEPTOR AGONISTS, at all costs.

[EDIT: To clarify, this is specifically in instances wherein the BLOOD BRAIN BARRIER (BBB) is compromised, which is in fact commonly the case with long-term sufferers of LYME DISEASE and its associated CO-INFECTIONS, wherein the pathogens have spread systemically and through the BBB into the CSF and BRAIN]

This is because such individuals will in all cases already be suffering from NMDA RECEPTOR OVERSTIMULATION; which is caused primarily by LYME DISEASE induced overproduction of QUINOLINIC ACID, an NMDA RECEPTOR AGONIST.

Individuals with or recovering from LYME DISEASE typically always suffer amongst their symptomatology COGNITIVE IMPAIRMENT, including BRAIN FOG, DIFFICULTY CONCENTRATING and MEMORY LOSS; caused (at least in part) by associated persistent NMDA RECEPTOR OVERSTIMULATION.

Consequently, such individuals should avoid any and all NMDA RECEPTOR AGONISTS, which would include D-SERINE.

Furthermore, since there exists ever increasing evidence that a significant (perhaps majority) percentage of people diagnosed as suffering from CHRONIC FATIGUE SYNDROME (CFS), MULTIPLE SCLEROSIS (MS), and/or MYALGIC ENCEPHALOMYELITIS (ME), in fact are suffering from LYME DISEASE (plus other associated CO-INFECTIONS) either in lieu of (in which case they have be misdiagnosed); or causally and hence concomitantly (in which case they have been incompletely diagnosed).

Therefore, individuals suffering from CFS, MS or ME are also strongly advised to avoid any and all NMDA RECEPTOR AGONISTS, including D-SERINE.

(N.B. The primary reason for the common occurrence of said diagnosis confusion is primarily due to the respective medical condition commonalities, specifically relating to the destruction of MYELIN SHEATHS, NERVE INFLAMMATION and/or DYSFUNCTION).

I should add that any and all such individuals might benefit from administration of an NMDA RECEPTOR ANTAGONIST, such as MAGNESIUM.

See the following for example:

Neurology. 1992 Jan;42(1):43-50.

Neuroactive kynurenines in Lyme borreliosis.

Halperin JJ, Heyes MP.

Source
Department of Neurology, SUNY, Stony Brook.

Abstract
Although neurologic dysfunction occurs frequently in patients with Lyme borreliosis, it is rarely possible to demonstrate the causative organism within the neuraxis. This discordance could arise if neurologic symptoms were actually due to soluble neuromodulators produced in response to infection. Since immune stimulation is associated with the production of quinolinic acid (QUIN), an excitotoxin and N-methyl-D-aspartate (NMDA) agonist, we measured levels of CSF and serum QUIN, and lymphokines. Samples were obtained from 16 patients with CNS Borrelia burgdorferi infection, eight patients with Lyme encephalopathy (confusion without intra-CNS inflammation), and 45 controls. CSF QUIN [quinolinic acid] was substantially elevated in patients with CNS Lyme and correlated strongly with CSF leukocytosis. In patients with encephalopathy, serum QUIN was elevated with corresponding increments in CSF QUIN. Lymphokine concentrations were not consistently elevated. We conclude that CSF QUIN [quinolinic acid] is significantly elevated in B burgdorferi infection--dramatically in patients with CNS inflammation, less in encephalopathy. The presence of this known agonist of NMDA synaptic function--a receptor involved in learning, memory, and synaptic plasticity--may contribute to the neurologic and cognitive deficits seen in many Lyme disease patients.

Edited by ScienceGuy, 26 August 2012 - 09:13 PM.

[Galantamine]

I do not believe in chronic lyme infection, and neither does the American Lyme Disease Foundation, so I'm in good company. If you'd like to discuss chronic lyme disease or any other pseudoscience, please start a new thread.

http://www.aldf.com/about.shtml
http://www.aldf.com/...conceptions.pdf
http://www.minnesota...38/Default.aspx
http://www.nejm.org/...y=T0enZgJwZtErw&
http://download.jour...34308001812.pdf
http://www.aldf.com/...dity_in_CLD.pdf
http://www.aldf.com/...ournal_2009.pdf
http://www.aldf.com/...nic_LD_2011.pdf
http://www.aldf.com/...ull_article.pdf (newer review)

[gizmobrain]

Regardless of the cause, his point is a valid one and worth mentioning: not everyone would benefit from increased NMDA firing. NMDA over-stimulation has been implicated in at least a few neuro conditions.

[Galantamine]

Regardless of the cause, his point is a valid one and worth mentioning: not everyone would benefit from increased NMDA firing. NMDA over-stimulation has been implicated in at least a few neuro conditions.

His point was that 1) chronic lyme diease exists, 2) chronic lyme disease predisposes to NMDA overstimulation, and 3) that many conditions are insidious representations of chronic lyme disease.

1) Chronic lyme disease does not exist.
2) Quinolinic acid does not cross the blood brain barrier (http://onlinelibrary...enticated=false) and would not be relevant for Lyme disease (save for neuroborreliosis, which is an acute exacerbation).
3) Chronic lyme disease is related to the aformentioned conditions only as a function of comorbid psychiatric illness which I linked to in the previous post.

Your point, however, is valid. People with genetic conditions (Huntington's disease), or those with a defective blood brain barrier (MS), among others, should consult a physician prior to engaging in this modality.

[unbeatableking]

ScienceGuy, although a 'nice' person in the general sense, isn't exactly known for his expertise on matters dealing with science, ironically.

BTW, I am under the assumption that DAA is a testosterone booster, would this fact be of any concern to women and those under the age of 21?

E-Pharm's Sarcosine/DAA blend is specifically marketed as such.

[CIMN]

"Your point, however, is valid. People with genetic conditions (Huntington's disease), or those with a defective blood brain barrier (MS), among others, should consult a physician prior to engaging in this modality."

-how does someone find out if their BBB is normal or abnormal?
seems most of the concerns regarding toxicity rest on the BBB system,

[unbeatableking]

Umm. Yeah. I think this issue has to be addressed.

There is no inherent danger with regards to D-Serine, but my main point of contention is the Sarcosine/DAA combo mentioned in this topic. It is pointed that the stack can lead to a rise in testosterone levels.

There are people after all, who would probably not want to experience this side-effect.

[gizmobrain]

Theoretically... it should act like this:

One' class='bbc_url' title='External link' rel='nofollow external'>http://www.silverhydra.com/2011/05/d-aspartic-acid-and-the-secret-to-italian-loving/']One thing that interested me throughout my research on D-AA was the ability of D-AA to act directly upon the aromatase enzyme. Theoretically this means that D-AA supplementation should increase active estrogens even if testosterone is not increased.
Upon further research, this has been noted in boars testes and in lizard ovaries. The aromatase enzyme does not differ in these animals and humans too significantly if at all, so it is possible that the same effects would be present in humans (still have to wait for studies in female humans though).
If this carries through to humans, then D-AA can be a compound which boosts test in men, and boosts estrogen in females. A truly multi-purpose supplement. Rather than ‘test booster’, D-AA is more akin to a ‘endocrine regulator’.

→ source (external link)

That page is a nice little summary of the theoretical implications of DAA on both the brain and the reproductive system.

The' class='bbc_url' title='External link' rel='nofollow external'>http://www.silverhydra.com/2011/05/d-aspartic-acid-and-the-secret-to-italian-loving/']The brain consists of D-Aspartate being converted into a very prominent signaling metabolite called NMDA (N-methyl-D-Aspartate). This influx of NMDA in the anterior pituitary and hypothalamus causes an acute secretion of Growth Hormone Releasing Hormone (GHRH), Prolactin releasing factors (PRFs), and Gonadotropin Releasing Hormone (GnRH). These hormones then induce production and secretion of Growth Hormone (GH), Prolactin, and both Follicle Stimulating hormone (FSH) and Luteinizing hormone (LH). (Another nice source) It’s basically an anabolic cascade. It also suppresses dopamine release (temporarily), so it’s not all perfect (and with the secretion of Prolactin, not too good of a combo for a prolonged period of time). Finally, it seems to induce release of both Melatonin-stimulating factor and GABA (a relaxing neurotransmitter) in the hypothalamus, suggesting that D-Aspartic acid would be better taken in the PM.

→ source (external link)

However, further discussion should probably find its way into a new thread.

Edited by zrbarnes, 26 August 2012 - 05:41 PM.

[unbeatableking]

Upvoted.

Hmm. The anecdotal reports of gynecomastia in addition to libido problems are somewhat discomforting.

It is important that we bring this issue out regardless of the extent to which it supposedly raises testosterone levels.

I myself am not concerned with the endocrinological ramifications of the compound, in fact, I am excited by this.

Just thought people should know what they are getting themselves into.

I shall wait for a response from Irish MD before I start a new thread.

Edited by unbeatableking, 26 August 2012 - 05:45 PM.

[Cognizant]

So, are we still waiting on someone to try the D-Serine/Sarcosine/DAA combo? I am very interested in this idea, especially since I have the DAA and I trust SmartPowders and would be all for using their D-Serine and Sarcosine. I also use NMDA antagonists (MagT and Glycine) at night and, so, I think that we could make a pretty good protocol (stylized in the Uridine/CILTEP stack way) of antagonists at night and positive modulators during the day, even adding in some AMPA allosteric modulators (like Aniracetam) for some serious receptor modulation.

[Psionic]

Regarding to NMDA overstimulation I wonder hows the effects of NMDA antagonists (alcohol, dissociatives) comparable to NMDA agonists mentioned here? Since I discovered their effects to be somewhat (but impairs some other processes/its related more to decisions making) memory-boosting and causing clear thoughts to arise (I got borreliosis some years ago), so can it be a sign that I have NMDA already overstimulated? Hows then effects of NMDA agonists to person with already overstimulated NMDA (worse short term memory/cognitive impairment)?

[ScienceGuy]

His point was that 1) chronic lyme diease exists, 2) chronic lyme disease predisposes to NMDA overstimulation, and 3) that many conditions are insidious representations of chronic lyme disease.

1) Chronic lyme disease does not exist.
2) Quinolinic acid does not cross the blood brain barrier (http://onlinelibrary...enticated=false) and would not be relevant for Lyme disease (save for neuroborreliosis, which is an acute exacerbation).
3) Chronic lyme disease is related to the aformentioned conditions only as a function of comorbid psychiatric illness which I linked to in the previous post.

Your point, however, is valid. People with genetic conditions (Huntington's disease), or those with a defective blood brain barrier (MS), among others, should consult a physician prior to engaging in this modality.

Erm... excuse me... but NO, my point was NOT in fact as you have stated.

Firstly, it is important to note that the term "Chronic Lyme Disease" is a misnomer; and consequently I prefer where possible to avoid using it. N.B. You will note that it is in fact YOU and not I that has chosen to use that particular term

Secondly, please kindly note that BORRELIOSIS (a.k.a. Lyme Disease) is practically impossible to contract by itself; wherein, in almost all cases it is contracted concurrently with other pathogens, including (but not limited to): BABESIOSIS and BARTONELLOSIS (as well as others); wherein there exists numerous differential strains for each and every.

Therefore, individuals who are incorrectly referred to as suffering from "Chronic Lyme Disease" will in fact be suffering from MULTIPLE PATHOGENIC INFECTIONS, including both BACTERIAL and PROTOZOAL; wherein, if / when left untreated said infections will spread SYSTEMICALLY into all the body's organs and eventually will pass through the BLOOD BRAIN BARRIER (BBB) into the CSF and BRAIN (NEUROBORRELIOSIS).

In such instances the integrity of the BBB becomes compromised and permeable (i.e. defective); and it is because of the DEFECTIVE BBB that the NMDA RECEPTOR OVERSTIMULATION is able to occur.

Hence, your statement "Quinolinic acid does not cross the blood brain barrier" is in fact akin to a red herring, since in such instances the BBB is defective.

Furthermore, RE: "Chronic lyme disease is related to the aformentioned conditions only as a function of comorbid psychiatric illness which I linked to in the previous post." - You need to delete the word "only" from that statement, since medical research has demonstrated that many MS, CFS and ME patients test positive for LYME DISEASE, which hence may be the underlying cause of the respective medical condition in those particular patients. This is a vital area of medicine that needs further research.

So, coming back to the topic of this thread, you need to accept that I am in fact correct in advising against use of NMDA RECEPTOR AGONISTS, which includes D-SERINE, in the instance wherein one is diagnosed as suffering from LYME DISEASE; however, I should clarify that this is particuarly applicable in the instance wherein the associated infection has been allowed to spread SYSTEMICALLY and into the CSF and BRAIN (NEUROBORELLIOSIS); and as such, when the BBB is defective. Although, it should be noted that DEFECTIVE BBB is in fact considerbly more common than you might think amongst LYME DISEASE sufferers; especially in cases wherein the infections are left undiagnosed and untreated for the long-term, as is tragically commonplace.

Furthermore, given the ever increasing indications that a significant percentage of individuals disagnosed as suffering from MS, CFS and/or ME are in fact infected with BORRELIOSIS (a.k.a. Lyme Disease) and its associated CO-INFECTIONS, it would be advisable for such individuals to also avoid use of NMDA RECEPTOR AGONISTS, which includes D-SERINE, especially if symptomatology associated with NMDA RECEPTOR OVERSTIMULATION is present

And well done for adding HUNTINGTON'S to that list

I do not believe in chronic lyme infection...

I don't either

Please kindly file "chronic lyme infection" in the same misnomer box as "Chronic Lyme Disease" for precisely the same reasons as stated above; i.e. there exists no such thing, because in such instances the reality is in fact NOT "chronic lyme infection", but MULTIPLE PATHOGENIC INFECTIONS with NEUROBORRELIOSIS.

Edited by ScienceGuy, 26 August 2012 - 09:26 PM.

[Galantamine]

You are still very incorrect, and I would ask you to please take this to another thread. Not only is lyme disease highly treatable, but it is self-resolving even without antibiotics for the greater majority of patients (demonstrated an enormous study by Yale University). Neuroborreliosis is exceptionally uncommon and is not related to BBB dysfunction.

Indeed lyme disease is often transmitted with other rickettsia, although they too are highly treatable, self-resolving for most, and have nothing to do with the BBB (they are RBC membranotrophic).

Suffice to say, your point is invalid and the evidence you have used is wrong, disorganized, out of context, and mildly humorous. I'm guessing, pre-med?

Regarding to NMDA overstimulation I wonder hows the effects of NMDA antagonists (alcohol, dissociatives) comparable to NMDA agonists mentioned here? Since I discovered their effects to be somewhat (but impairs some other processes/its related more to decisions making) memory-boosting and causing clear thoughts to arise (I got borreliosis some years ago), so can it be a sign that I have NMDA already overstimulated? Hows then effects of NMDA agonists to person with already overstimulated NMDA (worse short term memory/cognitive impairment)?

Oh for the love of god. I'm done with this forum.

[unbeatableking]

I think someone with a legitimate condition related to the CNS should speak to a primary health care professional prior to engaging in any sort of neurological supplementation.

With that being said, I honestly think this discussion regarding the dangers associated with d-serine use amongst abnormal populations should be discussed elsewhere. The substance has potential amongst normal individuals and its significance within that purview should be the main focus.

So please, any non-significant concerns should be taken elsewhere as it takes away from the overall discussion.

When I mean 'significant', I mean 'potentially harmful amongst normal individuals'. The nefiracetam testicular toxicity issue for example.

What ScienceGuy is doing is akin to butting into a thread regarding the use of methylphenidate or dextroamphetamine for study purposes and advising against their use amongst patients with bipolar disorders. Such a discussion can be taken elsewhere.

[gizmobrain]

Returning to the original intent of the thread, one thing that I've been wondering is about the glycine/d-serine co-agonism. So far, the only thing I've seen is that d-serine has a higher affinity at the glycine sites than glycine does. Is there any studies that would seem to point out that d-serine can be more beneficial than one of the many ways to raise glycine levels (glycine, sarcosine, trimethylglycine)?

[Cognizant]

Zrbarnes: Maybe I am reading this wrong (I probably am, as I am sure that this would not have been overlooked), but it looks like Glycine may not be the type of co-agonist that we thought it was, and may play a lesser role than previously thought. Honestly there is some strange, confusing information out there on this topic.
See:
http://www.ncbi.nlm....pubmed/16713567
http://www.ncbi.nlm....pubmed/18358625
http://www.ncbi.nlm....pubmed/17033043

"Removal of endogenous D-serine from slices was achieved by pretreating the tissue with recombinant D-serine deaminase enzyme. This enzyme is several orders of magnitude more efficient than previous methods to remove D-serine. We report that complete removal of D-serine virtually abolished NMDA-elicited neurotoxicity but did not protect against kainate. Although levels of glycine were 10-fold higher than D-serine, endogenous glycine was ineffective in mediating NMDA receptor neurotoxicity. The effect of endogenous glycine could be observed only after simultaneous removal of endogenous D-serine and blockage of the glycine transporter GlyT1. Our data indicate that D-serine is the dominant coagonist for NMDA receptor-elicited neurotoxicity, mediating all cell death elicited by NMDA in organotypic slices. The results suggest an essential role for this unusual D-amino acid, with implications for the mechanism of neuronal death in the nervous system." (as seen here: http://www.jneurosci...tent/25/41/9413)

Also, as for Sarcosine, it seems as though it may be more beneficial for NMDA receptor activation - "However, sarcosine differed from glycine because less NMDAR desensitization occurred with sarcosine than with glycine as the co-agonist." (as seen here: http://jp.physoc.org...87/13/3207.full)

Here is a giant review of the Glycine receptor of NMDA: http://pharmrev.aspe...7.full.pdf html

As for the comparison between the different chemicals, the chemicals in question have been compared for efficacy in the realm of cocaine conditioned place preference, which, according to http://www.ncbi.nlm....les/PMC2117900/ and http://www.ncbi.nlm....pubmed/21256147 involves NMDA receptors ("Using other behavioral models, evidence indicates that new learning is occurring during the extinction training experience [4,20,21]. This new learning may be dependent upon the activation of n-methyl-d-aspartate receptors (NMDARs), and either blocking NMDARs with antagonists or enhancing NMDAR activity with coagonists would be expected to affect the ability of an extinction training experience to alter the response to primed reinstatement. For example, conditioned fear has been used to demonstrate that NMDAR antagonists administered prior to extinction sessions can significantly inhibit extinction [2,10,22], and recent reports have indicated that treatment with D-cycloserine (an NMDAR coagonist) can facilitate extinction of conditioned fear [17,35]. Together, these findings indicate an involvement of NMDARs in the learning process that occurs during an extinction training experience.")
So, we are then looking for a comparison of the abilities of these chemicals to affect cocaine induced CPP and this may be what we are looking for: http://www.ncbi.nlm....pubmed/21106609


Also, this little gem about aging and D-Serine: http://www.ncbi.nlm....pubmed/20552041 and an article about the opposite approach (ie. NMDA antagonism) and its ability to increase "NMDAreceptors (NMDARs) signaling, BDNF expression, density of presynaptic puncta, and synaptic plasticity in the PFC but, interestingly, not in the basolateral amygdala" http://www.ncbi.nlm....pubmed/22016520