Uptake spill the beans.

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  1. Quote Originally Posted by jimbuick View Post
    Yep this is what I meant. My last weigh in was ~165 and I was hoping to get to a solid 175 by the end of this year, with this JRTC trip I don't expect that to happen but I would still like to get to 170 by Jan.
    Usually when someone tells me they want to gain 4-5 lbs. of lean mass in a short time frame, I am skeptical. In your situation, however, I think it's 100% achievable. After taking a month off of lifting your body is going respond well to the resistance training. Eating above maintenance and adding in the supps you plan to take should make it a reality.


  2. Quote Originally Posted by Dewey99

    Usually when someone tells me they want to gain 4-5 lbs. of lean mass in a short time frame, I am skeptical. In your situation, however, I think it's 100% achievable. After taking a month off of lifting your body is going respond well to the resistance training. Eating above maintenance and adding in the supps you plan to take should make it a reality.
    That's what I'm hoping, 4-5 in 2 months is definitely doable with no supps, I'm just hoping you guys can help me keep it a little leaner This is all very tentative still, the goals will obviously be reevaluated when I see what kind of condition I'm in when I come back.
    •   
       


  3. Just got the AN e-mail teaser for NO Uptake. Can not wait to see what pumptastic profile has been devised.

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    Always open light. Its not what you open with, its what you finish with. Louie Simmons

  4. Quote Originally Posted by AZMIDLYF View Post
    Just got the AN e-mail teaser for NO Uptake. Can not wait to see what pumptastic profile has been devised.

    Name:  Uptake%20Coming%20Soon%20Mad%20Mimi.jpg
Views: 272
Size:  237.0 KB
    Looks like some of the beans have been spilled....

  5. Quote Originally Posted by Dewey99

    Looks like some of the beans have been spilled....
    Are you gonna scoop them up and send them to me?
    •   
       


  6. Got my email too. Very curious to find out more!

  7. Quote Originally Posted by Dewey99

    Usually when someone tells me they want to gain 4-5 lbs. of lean mass in a short time frame, I am skeptical. In your situation, however, I think it's 100% achievable. After taking a month off of lifting your body is going respond well to the resistance training. Eating above maintenance and adding in the supps you plan to take should make it a reality.
    I wonder if I should take a month or two-3 weeks off. I only take one week every 6-8 weeks so like 4 weeks off a year basically... And even then o usually do one or two hit full body lifts that week... I can not grow no mo!!!

  8. Patiently waiting for more info.

    Sent from my MB865 using Am.com... LIKE A BOSS.
    SEMPER FI!!

  9. Quote Originally Posted by rms80 View Post
    NO Uptake are yellow capsules, but we also have another couple of betas that went into the same capsules, so it could be one of three things- we clearly label anything sent out, so it circumvents any issues. I tend to be pretty anal about labelling things- the guys in mfg. will tell you the same- I get pissed when I see unlabeled anything- especially when we have to go back and test it to figure out what it is.....
    Haha. I can attest to this. Everything is labeled!

    David
    Team APPNUT
    Applied Nutriceuticals Representative
    Appliednutriceuticals.com
    Are you ready for N.O. UPTAKE? It's a game-changer!

  10. just saw the email - do tell

  11. Right now I know of two products with yellow, one being N.O. Uptake the other a beta I've tested but gonna keep quiet. hehehe.
    By believing passionately in something that still does not exist, we create it. The nonexistent is whatever we have not sufficiently desired.
    Franz Kafka

  12. I saw DHEA on the label on the site, I hope that is a typo because DHEA orally is really estrogenic...
    doing my own thang!

  13. Quote Originally Posted by andrew732
    I saw DHEA on the label on the site, I hope that is a typo because DHEA orally is really estrogenic...
    Ditto this

  14. Quote Originally Posted by jimbuick View Post
    I'm going to JRTC on Wednesday for 30 days of no internet swamps....save me some?
    yes
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals

  15. Quote Originally Posted by andrew732 View Post
    I saw DHEA on the label on the site, I hope that is a typo because DHEA orally is really estrogenic...
    It has a really strong synergism with the NMDAR, if you are worried about estro (I wouldn't be with this), then stack it with Free Test
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals

  16. Quote Originally Posted by rms80
    yes
    Yeah buddy!
    Quote Originally Posted by rms80
    It has a really strong synergism with the NMDAR, if you are worried about estro (I wouldn't be with this), then stack it with Free Test
    Ill stack it with free test, if I can afford it lol.

  17. Quote Originally Posted by rms80 View Post
    It has a really strong synergism with the NMDAR, if you are worried about estro (I wouldn't be with this), then stack it with Free Test
    Are you referring to DAA's ability to increase NMDA receptor binding sites? It may good for nootropics, but may not be the case for hormones especially post usage...
    doing my own thang!

  18. Quote Originally Posted by rms80 View Post
    It has a really strong synergism with the NMDAR, if you are worried about estro (I wouldn't be with this), then stack it with Free Test
    Quote Originally Posted by andrew732 View Post
    I saw DHEA on the label on the site, I hope that is a typo because DHEA orally is really estrogenic...
    It has a really strong synergism with the NMDAR, if you are worried about estro, then stack it with Free Test- they stack phenomenally. The androst-35-dien-7,17-dione in FT is a strong AI, and forskolin increases 3B-HSD (increases conversion of DHEA to Androstenedione)....read below and it will make more sense:

    How N.O. Uptake™ Increases Testosterone and GH Levels Through the NMDA Receptor: The Role of N-Methyl D-,L-Aspartate, DHEA, and N,N,N-Methylglycine (TMG Nitrate)

    • The first mechanism of action in N.O. Uptake™ has to do with three entities: the NMDAR (N-Methyl D-Aspartate) receptor, the biochemical pathway concerning SAM-e production and methylation which also acts as a co-ligand for the NMDAR, and the action of DHEA in priming NMDAR stimulation; creating a distinct and complex synergistic effect created by both direct stimulation and interaction of the three.
    • NMDAR are found through the nervous system, and have a role in learning, memory, and the endocrine system. When NMDAR receptors are bound by their specific ligands and co-ligands in the hypothalamus, a hormonal cascade begins, ultimately allowing for the release of GH and Testosterone downstream.
    • The SAM-e / methylation pathway is responsible for a variety of different biochemical reactions in the body. In Uptake™ the SAM-e pathway is responsible for the de-methylation of TMG to sarcosine (n-methylglycine, an important co-ligand of the NMDAR), plus the formation of HS, both of which allow for greater NMDAR activity, greater NO activity (and HS synergism), leading to ultimately greater initiation of hormonal release (1,37,52,53).



    • The NMDAR is pretty tricky, in that it requires more than one component to activate the receptor (called ligands). Ligands are molecules that act as a trigger on a target entity (receptor) to activate a biological process. There are two crucial binding sites on NMDA receptors where ligands can exert strong activity: the glycine binding site (NR-1), and the NMDA binding site (NR-2) (39,40,41,47).
    • The ligand with the strongest affinity (ability to bind to) for the NR-2 site in the hypothalamus is D-Aspartic Acid, while the ligand with the strongest affinity for the NR-1 binding site is n-methyl glycine (also known as sarcosine). To recap, the ligand with the strongest ability to bind the NMDA binding site (NR-2) in the hypothalamus is D-Aspartic Acid (followed by N-Methyl D-Aspartic Acid, which is in N.O. Uptake™), and the ligand with the strongest ability to bind the glycine binding site (NR-1) is n-methyl glycine (34,36,38).
    • This is noteworthy, in that the type of ligand that binds to the NR-1 binding site determines the response of the receptor. L-Glycine binds to the site quite well, but is not a good choice for our task, because it is rapidly removed from the binding site by glycine transporter 1 (GT1), a transport protein that regulates the re-uptake of glycine from the synapse (the space between nerve cells). GT1 determines the amount of glycine present between nerve endings; greater GT1 activity allows for less glycine buildup in the synapse, and the more glycine that is removed from the synapse, the less effective it can be as a co-agonist in activating the NMDA receptor. Since NMDA reception must be co-activated by two separate ligands, if one is ineffective or removed too quickly there will be little or no activation occurring, which would lead to a less effective product (33,34,64).
    • Therefore, the goal is to find another ligand that can bind the GT1 and block or slow the action of the transporter protein. Blocking or slowing the action of GT1 allows greater amounts of glycine build-up in and around the synapse, which will allow for increased activation of the NR-1 binding site. This, along with the docking of N-Methyl D-Aspartic Acid on the NR-2 binding site, is essential for attaining the strongest activation of the NMDAR. D-Serine, D-Alanine, D-Cycloserine, and Sarcosine (N-Methyl Glycine, or demethylated TMG NItrate) are compounds that come to mind for this purpose; each of these compounds can act as a decent ligand of the NR-1 binding site. N-Methyl Glycine (Sarcosine) is the best choice for this job, because it limits GT1 action, slowing the removal of glycine from the synapse. Another reason sarcosine is a good choice has to do with its’ ability to act as a ligand/co-agonist of the NR-1 binding site. This means that N-Methyl Glycine can also act on the NR-1 glycine receptor as well as GT1, making it a very effective co-agonist to the NMDAR. When both NR-1 and NR-2 have been successfully bound with lower glycine transporter (GT1) activity, better overall stimulation of the NMDAR will happen, which can allow for a maximal physiological response and optimal product effectiveness (65,66).
    • However, yet another compound, N,N,N-trimethylglycine (TMG Nitrate) serves a multi-faceted function in a similar way to N-Methyl Glycine, D-Alanine, and D-Serine. TMG Nitrate can be directly converted by the liver to the NR-1 agonist N-Methyl Glycine (Sarcosine), meaning that N.O. Uptake™ effectively allows for a co-agonist of the NMDAR to be present. However, TMG Nitrate must first undergo a simple enzymatic conversion In becoming sarcosine (n-methylglycine), which is accomplished by acting as a methyl donor. (See Figure 4 below). This means that TMG donates extra methyl groups to other molecules through the methylation pathway and offers some additional benefits to N.O. Uptake™, as the methylation pathway is responsible for the production of neurotransmitters, the structure and function of DNA, and the metabolism of fats. The conversion of TMG Nitrate to N-Methyl Glycine (sarcosine) is very efficient, giving N.O. Uptake™ excellent co-ligand enhancement for the NMDAR to work in conjunction with N-Methyl D-Aspartic Acid on NR-1 and NR-2 (35,38,47,56,62,63,65,66).
    • When the NMDAR binding sites are triggered in the hypothalamus by NMDA and its co-agonist (in this case N-Methyl Glycine), there is an increase in cyclic guanosine monophosphate (cGMP) activity in the pituitary. cGMP is classified as a second messenger, meaning that it exerts its effects by acting in a manner secondary and in response to a first messenger signaling molecule. When the first messenger signaling molecules bind to a receptor (in this case, NMDA and its co-agonist bind to NR-1 and NR-2), the secondary pathway is activated that increases cGMP production. The heightened levels of cGMP in the pituitary correspond to an increased production of gonadotropin releasing hormone (GnRH), and growth hormone releasing hormone (GHRH). The resulting increase in GHRH from stimulation of the NMDA receptor also allows increased amounts of growth hormone (GH) to be secreted from the pituitary (5,54,55,67).
    • As aforementioned, GnRH release also occurs, signaling the pituitary to release luteinizing hormone (LH), and follicle stimulating hormone (FSH) (see figure 2). Certain neurosteroids such as Pregnenolone Sulfate and DHEA have been shown to have significant positive influence on the N-Methyl D-Aspartate receptor. DHEA can further potentiate the release of GnRH through the NMDA receptor, as the effect of DHEA on the release of GnRH induced by glutamate is consistent with the identity of DHEA as a positive modulator of the NMDAR. This increase in GnRH activity, and the resultant increase in LH and FSH release, allows for an upregulation of steroidogenesis by the testes, which subsequently allows for the production of increased amounts of testosterone, as explained below (5,67,140),
    • Luteinizing Hormone, through receptors found on the Leydig cells (a type of cell that helps produce testosterone) in the testes, has control over the production and secretion of testosterone. The subsequent binding of LH with its receptor on the Leydig cell allows a signal to be sent through the cyclic AMP (cAMP, another type of second messenger) pathway. Once this signaling occurs, the protein kinase A pathway is then activated, and this ultimately allows for the release of testosterone after 30-60 minutes of LH stimulation (2,3,34-36,72,73).
    • Similarly, increases in cGMP from N.O. Uptake™ also enhance phosphorylation (a fancy word for activation via attachment of a phosphate group) of the steroidogenic acute regulatory protein (StAR), a Leydig cell cholesterol transfer protein that provides the building blocks for testosterone synthesis. This is important for increasing endogenous testosterone production, in that StAR activation is necessary for the stimulation of steroidogenic enzymes involved in the transfer of cholesterol to testosterone. These results suggest that increases in cGMP correlate to increases in basal steroidogenesis in the Leydig cells of the testes through the protein kinase G (PKG, or a type of enzyme that cGMP interacts with)-dependent modification of the StAR protein and interaction with LH. To summarize N.O. Uptake increases LH, cGMP, and StAR activity, all of which can significantly up the amount of testosterone produced in the body (72,73).
    • As you can see in Figure 5 (below), TMG Nitrate functions within the pathway SAM-e, albeit in different segments and capacities; each of which add to product effectiveness. TMG Nitrate has been shown have positive effects on muscular strength it can increase creatine storage and synthesis, as well as having the ability to be transformed into sarcosine (an NMDAR co-ligand) and act as a methyl donor to fuel SAM-e formation and ultimately increase HS levels (a synergistic donor gas similar to NO). TMG Nitrate acts in the following fashion as a methyl donor and in the SAM-e pathway (57,59,60,61,84-87):
      • TMG donates a methyl group during the formation of SAM-e, and becomes DMG (N-N-dimethylglycine).
      • The donated methyl group can then form SAM-e, or be used for the production of neurotransmitters, the production of DNA, or the metabolism of fats
      • The remaining DMG is then converted readily by the liver to the NR-1 agonist N-Methyl Glycine via glycine N-methyltransferase.
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals

  19. Quote Originally Posted by andrew732 View Post
    Are you referring to DAA's ability to increase NMDA receptor binding sites? It may good for nootropics, but may not be the case for hormones especially post usage...
    The product doesn't contain DAA- it contains NMA (N-Methyl D-,L-Aspartic Acid); and this isn't a PCT product
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals

  20. Quote Originally Posted by rms80 View Post
    The product doesn't contain DAA- it contains NMA (N-Methyl D-,L-Aspartic Acid); and this isn't a PCT product
    They will most likely put the full tech-write up on the website- it explains the entire product in detail and all of the reasoning behind the compounds and MOAs
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals

  21. Can't wait!

    Sent from my MB865 using Am.com... LIKE A BOSS.
    SEMPER FI!!

  22. Quote Originally Posted by rms80 View Post
    The product doesn't contain DAA- it contains NMA (N-Methyl D-,L-Aspartic Acid); and this isn't a PCT product
    I meant to say DHEA. Also, even though it isn't a ph product, its claim is to boost endogenous testosterone but I sense there could be an issue for some and not all.
    doing my own thang!

  23. Quote Originally Posted by enhanced
    Can't wait!

    Sent from my MB865 using Am.com... LIKE A BOSS.
    Me neither!!
    After a year off, I'm back

  24. Quote Originally Posted by enhanced View Post
    Can't wait!

    Sent from my MB865 using Am.com... LIKE A BOSS.
    Why wait? Win a promo and get it!

    Out from the shadows - INBF World Championships 2012
    By believing passionately in something that still does not exist, we create it. The nonexistent is whatever we have not sufficiently desired.
    Franz Kafka

  25. Quote Originally Posted by rms80 View Post
    It has a really strong synergism with the NMDAR, if you are worried about estro, then stack it with Free Test- they stack phenomenally. The androst-35-dien-7,17-dione in FT is a strong AI, and forskolin increases 3B-HSD (increases conversion of DHEA to Androstenedione)....read below and it will make more sense:

    How N.O. Uptake™ Increases Testosterone and GH Levels Through the NMDA Receptor: The Role of N-Methyl D-,L-Aspartate, DHEA, and N,N,N-Methylglycine (TMG Nitrate)

    • The first mechanism of action in N.O. Uptake™ has to do with three entities: the NMDAR (N-Methyl D-Aspartate) receptor, the biochemical pathway concerning SAM-e production and methylation which also acts as a co-ligand for the NMDAR, and the action of DHEA in priming NMDAR stimulation; creating a distinct and complex synergistic effect created by both direct stimulation and interaction of the three.
    • NMDAR are found through the nervous system, and have a role in learning, memory, and the endocrine system. When NMDAR receptors are bound by their specific ligands and co-ligands in the hypothalamus, a hormonal cascade begins, ultimately allowing for the release of GH and Testosterone downstream.
    • The SAM-e / methylation pathway is responsible for a variety of different biochemical reactions in the body. In Uptake™ the SAM-e pathway is responsible for the de-methylation of TMG to sarcosine (n-methylglycine, an important co-ligand of the NMDAR), plus the formation of HS, both of which allow for greater NMDAR activity, greater NO activity (and HS synergism), leading to ultimately greater initiation of hormonal release (1,37,52,53).



    • The NMDAR is pretty tricky, in that it requires more than one component to activate the receptor (called ligands). Ligands are molecules that act as a trigger on a target entity (receptor) to activate a biological process. There are two crucial binding sites on NMDA receptors where ligands can exert strong activity: the glycine binding site (NR-1), and the NMDA binding site (NR-2) (39,40,41,47).
    • The ligand with the strongest affinity (ability to bind to) for the NR-2 site in the hypothalamus is D-Aspartic Acid, while the ligand with the strongest affinity for the NR-1 binding site is n-methyl glycine (also known as sarcosine). To recap, the ligand with the strongest ability to bind the NMDA binding site (NR-2) in the hypothalamus is D-Aspartic Acid (followed by N-Methyl D-Aspartic Acid, which is in N.O. Uptake™), and the ligand with the strongest ability to bind the glycine binding site (NR-1) is n-methyl glycine (34,36,38).
    • This is noteworthy, in that the type of ligand that binds to the NR-1 binding site determines the response of the receptor. L-Glycine binds to the site quite well, but is not a good choice for our task, because it is rapidly removed from the binding site by glycine transporter 1 (GT1), a transport protein that regulates the re-uptake of glycine from the synapse (the space between nerve cells). GT1 determines the amount of glycine present between nerve endings; greater GT1 activity allows for less glycine buildup in the synapse, and the more glycine that is removed from the synapse, the less effective it can be as a co-agonist in activating the NMDA receptor. Since NMDA reception must be co-activated by two separate ligands, if one is ineffective or removed too quickly there will be little or no activation occurring, which would lead to a less effective product (33,34,64).
    • Therefore, the goal is to find another ligand that can bind the GT1 and block or slow the action of the transporter protein. Blocking or slowing the action of GT1 allows greater amounts of glycine build-up in and around the synapse, which will allow for increased activation of the NR-1 binding site. This, along with the docking of N-Methyl D-Aspartic Acid on the NR-2 binding site, is essential for attaining the strongest activation of the NMDAR. D-Serine, D-Alanine, D-Cycloserine, and Sarcosine (N-Methyl Glycine, or demethylated TMG NItrate) are compounds that come to mind for this purpose; each of these compounds can act as a decent ligand of the NR-1 binding site. N-Methyl Glycine (Sarcosine) is the best choice for this job, because it limits GT1 action, slowing the removal of glycine from the synapse. Another reason sarcosine is a good choice has to do with its’ ability to act as a ligand/co-agonist of the NR-1 binding site. This means that N-Methyl Glycine can also act on the NR-1 glycine receptor as well as GT1, making it a very effective co-agonist to the NMDAR. When both NR-1 and NR-2 have been successfully bound with lower glycine transporter (GT1) activity, better overall stimulation of the NMDAR will happen, which can allow for a maximal physiological response and optimal product effectiveness (65,66).
    • However, yet another compound, N,N,N-trimethylglycine (TMG Nitrate) serves a multi-faceted function in a similar way to N-Methyl Glycine, D-Alanine, and D-Serine. TMG Nitrate can be directly converted by the liver to the NR-1 agonist N-Methyl Glycine (Sarcosine), meaning that N.O. Uptake™ effectively allows for a co-agonist of the NMDAR to be present. However, TMG Nitrate must first undergo a simple enzymatic conversion In becoming sarcosine (n-methylglycine), which is accomplished by acting as a methyl donor. (See Figure 4 below). This means that TMG donates extra methyl groups to other molecules through the methylation pathway and offers some additional benefits to N.O. Uptake™, as the methylation pathway is responsible for the production of neurotransmitters, the structure and function of DNA, and the metabolism of fats. The conversion of TMG Nitrate to N-Methyl Glycine (sarcosine) is very efficient, giving N.O. Uptake™ excellent co-ligand enhancement for the NMDAR to work in conjunction with N-Methyl D-Aspartic Acid on NR-1 and NR-2 (35,38,47,56,62,63,65,66).
    • When the NMDAR binding sites are triggered in the hypothalamus by NMDA and its co-agonist (in this case N-Methyl Glycine), there is an increase in cyclic guanosine monophosphate (cGMP) activity in the pituitary. cGMP is classified as a second messenger, meaning that it exerts its effects by acting in a manner secondary and in response to a first messenger signaling molecule. When the first messenger signaling molecules bind to a receptor (in this case, NMDA and its co-agonist bind to NR-1 and NR-2), the secondary pathway is activated that increases cGMP production. The heightened levels of cGMP in the pituitary correspond to an increased production of gonadotropin releasing hormone (GnRH), and growth hormone releasing hormone (GHRH). The resulting increase in GHRH from stimulation of the NMDA receptor also allows increased amounts of growth hormone (GH) to be secreted from the pituitary (5,54,55,67).
    • As aforementioned, GnRH release also occurs, signaling the pituitary to release luteinizing hormone (LH), and follicle stimulating hormone (FSH) (see figure 2). Certain neurosteroids such as Pregnenolone Sulfate and DHEA have been shown to have significant positive influence on the N-Methyl D-Aspartate receptor. DHEA can further potentiate the release of GnRH through the NMDA receptor, as the effect of DHEA on the release of GnRH induced by glutamate is consistent with the identity of DHEA as a positive modulator of the NMDAR. This increase in GnRH activity, and the resultant increase in LH and FSH release, allows for an upregulation of steroidogenesis by the testes, which subsequently allows for the production of increased amounts of testosterone, as explained below (5,67,140),
    • Luteinizing Hormone, through receptors found on the Leydig cells (a type of cell that helps produce testosterone) in the testes, has control over the production and secretion of testosterone. The subsequent binding of LH with its receptor on the Leydig cell allows a signal to be sent through the cyclic AMP (cAMP, another type of second messenger) pathway. Once this signaling occurs, the protein kinase A pathway is then activated, and this ultimately allows for the release of testosterone after 30-60 minutes of LH stimulation (2,3,34-36,72,73).
    • Similarly, increases in cGMP from N.O. Uptake™ also enhance phosphorylation (a fancy word for activation via attachment of a phosphate group) of the steroidogenic acute regulatory protein (StAR), a Leydig cell cholesterol transfer protein that provides the building blocks for testosterone synthesis. This is important for increasing endogenous testosterone production, in that StAR activation is necessary for the stimulation of steroidogenic enzymes involved in the transfer of cholesterol to testosterone. These results suggest that increases in cGMP correlate to increases in basal steroidogenesis in the Leydig cells of the testes through the protein kinase G (PKG, or a type of enzyme that cGMP interacts with)-dependent modification of the StAR protein and interaction with LH. To summarize N.O. Uptake increases LH, cGMP, and StAR activity, all of which can significantly up the amount of testosterone produced in the body (72,73).
    • As you can see in Figure 5 (below), TMG Nitrate functions within the pathway SAM-e, albeit in different segments and capacities; each of which add to product effectiveness. TMG Nitrate has been shown have positive effects on muscular strength it can increase creatine storage and synthesis, as well as having the ability to be transformed into sarcosine (an NMDAR co-ligand) and act as a methyl donor to fuel SAM-e formation and ultimately increase HS levels (a synergistic donor gas similar to NO). TMG Nitrate acts in the following fashion as a methyl donor and in the SAM-e pathway (57,59,60,61,84-87):
      • TMG donates a methyl group during the formation of SAM-e, and becomes DMG (N-N-dimethylglycine).
      • The donated methyl group can then form SAM-e, or be used for the production of neurotransmitters, the production of DNA, or the metabolism of fats
      • The remaining DMG is then converted readily by the liver to the NR-1 agonist N-Methyl Glycine via glycine N-methyltransferase.
    Great write up!!
    After a year off, I'm back
  •   

      
     

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