Namenda response

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FatherOf2
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Re: Namenda response

Postby FatherOf2 » Thu May 25, 2017 9:41 am

luis wrote:Bump.
Fo2, is your son still on Namenda ? My son is almost 17 and for the last 2 years we have been struggling against violent behaviors, coinciding with adolescence.
I suspected and confirmed that testosterone increases glutamate excitotoxicity (I can find the link if it interests anyone).
From one side there is that Theory of autistics being the super-male, excessive testosterone etc.
From other side, there is the 2012 Bumetanide study, that is still increasing in importance, with double blind/placebo tests being done all over the world, including China, very recently. Excess intracellular chlorine inverting GABA's funtion, from inhibitory to excitatory.
My son is on Bumetanide, and I was thinking if now would it be a good time to try Namenda again.
Only brainstorming: maybe Namenda's effect didn't fix because of excessive chlorine in neurons ? Maybe combining Namenda with Bumetanide could be good ? Maybe trying to reduce testosterone (with inositol and flaxseed powder) could help even more ?
Maybe avoiding supplements that increase glutamate, like B12, and taking others that help to reduce it, like lithium, could help even more ?

I would appreciate others thinking about this (not only Fo2), please.
Maybe we can help each other here exchanging our thoughts.

Thank you.

Namenda caused irritability in my son twice. But everyone is different. Other than that side effect, it was great for social. I wouldn't recommend it though, because I haven't heard of people using it for anger management. My recommendation would be

Verapamil will be on the top of my list due to some parents swearing by its calming properties.
Continue Bumetanide.
Try Flaxseed oil (anti-androgen).
Try Reishi mushrooms (strong anti-androgen + immune balancing, specifically mentioned its calming properties).
Try Lithium, but ionic. I never tried ionic, but Lithium orotate doesn't work on my son.
Try Manganese to regulate blood sugar levels.
Trileptal was very good for us in balancing the mood.
Talk to psychiatrist about using SSRI for anger off-label. My son just started it. He became very happy and more social boy.
Last edited by FatherOf2 on Thu May 25, 2017 10:35 am, edited 1 time in total.

luis
Posts: 257
Joined: Thu Sep 25, 2008 8:42 pm

Re: Namenda response

Postby luis » Thu May 25, 2017 9:58 am

FatherOf2 wrote:Namenda caused irritability in my son twice. But everyone is different. Other than that side effect, it was great for social. I wouldn't recommend it though, because I haven't heard of people using it for anger management. My recommendation would be

Verapamil will be on the top of my list due to some parents swearing by its calming properties.
Continue Bumetanide.
Try Flaxseed oil (anti-androgen).
Try Reishi mushrooms (strong anti-androgen + immune balancing, specifically mentioned its calming properties).
Try Lithium, but ionic. I never tried ionic, but Lithium orotate doesn't work on my son.
Try Manganese to regulate blood sugar levels.
Talk to psychiatrist about using SSRI for anger off-label. My son just started it. He became very happy and more social boy.


Thank you, Fo2 ! Very interesting tip about Verapamil. I've just read about it on Wikipedia, and it seems very appropriate. I'll give it a try.
I'm already using flaxseed flour, instead of oil, because my son has problems with oils (very sensitive duodenum). It seems to help calm him down.
I'm already using Ionic Lithium (New Beginnings, very good).
Using Manganese, too. Ionic, from BodyBio. My son has high piruvate.

Do you know if Reishi mushrooms have glutamate ? It seems that all mushrooms have but I may be wrong.
Thanks, again !! :)

FatherOf2
Posts: 1668
Joined: Mon Mar 11, 2013 1:37 am

Re: Namenda response

Postby FatherOf2 » Thu May 25, 2017 10:39 am

It is not immediately clear to me that glutamate is the problem. I am actually thinking of trying Sarcosine, which should help with cognition and mood. My son has DOA mutation that reduces D-Serine, and Sarcosine is supposed to help with that (reduces breakdown of glycine, which acts as co-agonist at NMDA in manner similar to D-Serine; the other agonist is glutamate). Schizophrenia is now often thought to be caused by low activity of NMDA. There are many on-going studies of Sarcosine as an effective treatment of Schizophrenia (Sarcosine is a sweet-powder supplement, produced in your body naturally). Glycine is not only coagonist of NMDA receptors, but also an inhibitory neurotransmitter like GABA.

luis
Posts: 257
Joined: Thu Sep 25, 2008 8:42 pm

Re: Namenda response

Postby luis » Fri May 26, 2017 8:36 am

FatherOf2 wrote:It is not immediately clear to me that glutamate is the problem. I am actually thinking of trying Sarcosine, which should help with cognition and mood. My son has DOA mutation that reduces D-Serine, and Sarcosine is supposed to help with that (reduces breakdown of glycine, which acts as co-agonist at NMDA in manner similar to D-Serine; the other agonist is glutamate). Schizophrenia is now often thought to be caused by low activity of NMDA. There are many on-going studies of Sarcosine as an effective treatment of Schizophrenia (Sarcosine is a sweet-powder supplement, produced in your body naturally). Glycine is not only coagonist of NMDA receptors, but also an inhibitory neurotransmitter like GABA.


Fo2, sorry, but you have completely changed your mind regarding blocking NMDA to be a good thing ?
Rememore, in the previous posts, in this same topic, you've told us how better your son has got since taking Namenda. (Later, you've found out that the gains did not stick).
Please, let me understand it. Now you think that it is good to increase NMDA activiy ?

FatherOf2
Posts: 1668
Joined: Mon Mar 11, 2013 1:37 am

Re: Namenda response

Postby FatherOf2 » Fri May 26, 2017 9:57 am

luis wrote:Fo2, so you have completely changed your mind regarding blocking NMDA to be a good thing ?
Remember, in the previous posts, in this same topic, you've told us how better your son has got since taking Namenda. (Later, you've found out that the gains did not stick).
Please, let me understand it. Now you think that it is good to increase NMDA activiy ?

I am just a parent like you. I don't have the authority over "the right thing to do", which in the case of autism is different for different child. I will explain my thought process. Glutamate is an excitatory neurotransmitter, which acts as a key to open ion channels in NMDA receptors for Calcium ions to come into a neuron body and make it fire. But the channels need also co-agonist to be open, either Glycine or D Serine. In some cases, like Alzheimers or ADHD or seizures, there is too much excitation (or firing) of neurons, that it leads to its death, or hyperactivity, or seizures. All these are bad things, which clearly dictate the need to reduce Glutamate or Calcium or block NMDA receptors with something like Magnesium or Namenda.

So far the picture is clear and non-controversial. Except for one thing: schizophrenia. Autism used to be diagnosed as "childhood schizophrenia". And if you find an old-enough psychiatrist, who worked in 70's and 80's, he/she will confirm that. The word of autism was coined by a British researcher, who showed that auitsm, as we know it today, is different from schizophrenia because it doesn't have elements of hallucination, paranoia of being in danger, and persistence of thoughts. Or does it? When an autistic child day dreams or talks to himself, is that a hallucination?
Today the diagnosis of schizophrenia can only be given when the child reaches adolescence, and some cases of autism will become re-diagnosed as schizophrenia.

In the past, schizophrenia was assumed to be caused by overactive D2 dopamine receptors and some serotonin receptors. Antipsychotic drugs such as Risperidone or Abilify are based on blocking those receptors. By the way, if autism is not schizophrenia, why the only approved drugs for autism are those used to treat schizophrenia. And I am NOT saying that autism = schizophrenia, I am just making an observation. But the above mentioned antipsychotic drugs have one thing in common: they negatively affect cognition, which is already low (a negative symptom) in schizophrenia. Recently, it was discovered through postmortem brains analysis of schizophrenia patients that they have one thing in common: low D serine levels. Key mutations were identified common between schizophrenia patients: some are related to lack of production or excessive break down of D Serine. Wait a second. D Serine should be bad because it is co-agonist of NMDA receptors, just like Glutamate, right? How could it be that lack of NMDA excitation causes schizophrenia, which in early stages diagnosed as autism. There are several clinical studies researching Sarcosine or its analogs as novel treatments of schizophrenia. Those substances prevent breakdown of Glycine, which acts D Serine. WHat they disovered in some studies already is that raising Glycine levels not only improves positive symptoms (mood) of schizophrenia, but negative symptoms (mood) as well. That is why opinion about NMDA receptors is not one way (need to block) or the other (need to agonize). One thing is clear, that low activity of NMDA is bad too and causes schizophrenia and other disorders. So, like everything in this life, perhaps activity of NMDA receptors has to be balanced, or in a certain optimum range, not too high (which would cause sezires, neuronal death, hyperactivity) or too low (which would cause poor cognition, mood, schizophrenia).

luis
Posts: 257
Joined: Thu Sep 25, 2008 8:42 pm

Re: Namenda response

Postby luis » Fri May 26, 2017 11:07 am

FatherOf2 wrote:
luis wrote:Fo2, so you have completely changed your mind regarding blocking NMDA to be a good thing ?
Remember, in the previous posts, in this same topic, you've told us how better your son has got since taking Namenda. (Later, you've found out that the gains did not stick).
Please, let me understand it. Now you think that it is good to increase NMDA activiy ?

I am just a parent like you. I don't have the authority over "the right thing to do", which in the case of autism is different for different child. I will explain my thought process. Glutamate is an excitatory neurotransmitter, which acts as a key to open ion channels in NMDA receptors for Calcium ions to come into a neuron body and make it fire. But the channels need also co-agonist to be open, either Glycine or D Serine. In some cases, like Alzheimers or ADHD or seizures, there is too much excitation (or firing) of neurons, that it leads to its death, or hyperactivity, or seizures. All these are bad things, which clearly dictate the need to reduce Glutamate or Calcium or block NMDA receptors with something like Magnesium or Namenda.

So far the picture is clear and non-controversial. Except for one thing: schizophrenia. Autism used to be diagnosed as "childhood schizophrenia". And if you find an old-enough psychiatrist, who worked in 70's and 80's, he/she will confirm that. The word of autism was coined by a British researcher, who showed that auitsm, as we know it today, is different from schizophrenia because it doesn't have elements of hallucination, paranoia of being in danger, and persistence of thoughts. Or does it? When an autistic child day dreams or talks to himself, is that a hallucination?
Today the diagnosis of schizophrenia can only be given when the child reaches adolescence, and some cases of autism will become re-diagnosed as schizophrenia.

In the past, schizophrenia was assumed to be caused by overactive D2 dopamine receptors and some serotonin receptors. Antipsychotic drugs such as Risperidone or Abilify are based on blocking those receptors. By the way, if autism is not schizophrenia, why the only approved drugs for autism are those used to treat schizophrenia. And I am NOT saying that autism = schizophrenia, I am just making an observation. But the above mentioned antipsychotic drugs have one thing in common: they negatively affect cognition, which is already low (a negative symptom) in schizophrenia. Recently, it was discovered through postmortem brains analysis of schizophrenia patients that they have one thing in common: low D serine levels. Key mutations were identified common between schizophrenia patients: some are related to lack of production or excessive break down of D Serine. Wait a second. D Serine should be bad because it is co-agonist of NMDA receptors, just like Glutamate, right? How could it be that lack of NMDA excitation causes schizophrenia, which in early stages diagnosed as autism. There are several clinical studies researching Sarcosine or its analogs as novel treatments of schizophrenia. Those substances prevent breakdown of Glycine, which acts D Serine. WHat they disovered in some studies already is that raising Glycine levels not only improves positive symptoms (mood) of schizophrenia, but negative symptoms (mood) as well. That is why opinion about NMDA receptors is not one way (need to block) or the other (need to agonize). One thing is clear, that low activity of NMDA is bad too and causes schizophrenia and other disorders. So, like everything in this life, perhaps activity of NMDA receptors has to be balanced, or in a certain optimum range, not too high (which would cause sezires, neuronal death, hyperactivity) or too low (which would cause poor cognition, mood, schizophrenia).


Thank you, Fo2.
Well, I'll have to study about this. It's new to me. It makes sense. Maybe it depends on the situation of the patient.
At this moment, I guess that my son needs more inhibition of NMDA receptors and more control of glutamate. (I read yesterday that some virus block the GAD enzyme, that is supposed to convert glutamate to GABA. And my son is definitely a virus boy.)

This is hard for me to understand. When my son takes supplements that increase glutamate, his speech increase a lot. But also his irritability and, on the limit, aggression. As you said, glutamate increases cognition. But it also increases inflammation.
Maybe what I need is to control virus better.

Thanks, again, Fo2.

FatherOf2
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Joined: Mon Mar 11, 2013 1:37 am

Re: Namenda response

Postby FatherOf2 » Fri May 26, 2017 7:37 pm

luis wrote:Thank you, Fo2.
Well, I'll have to study about this. It's new to me. It makes sense. Maybe it depends on the situation of the patient.
At this moment, I guess that my son needs more inhibition of NMDA receptors and more control of glutamate. (I read yesterday that some virus block the GAD enzyme, that is supposed to convert glutamate to GABA. And my son is definitely a virus boy.)

This is hard for me to understand. When my son takes supplements that increase glutamate, his speech increase a lot. But also his irritability and, on the limit, aggression. As you said, glutamate increases cognition. But it also increases inflammation.
Maybe what I need is to control virus better.

Thanks, again, Fo2.

We have very similar sons. My son too reacts very positively to glutamate boosting at first, but then irritability increases. Goldenseal does it for him. Whether my son's irritability is related to increased glutamate or something else remains to be answered. After all, Goldenseal has multiple actions, one of which is killing yeast. The fact that irritability from Goldenseal starts about 1 week after starting Goldenseal tells me that it might be related to changing gut flora (bad bacteria taking over small intestine, or something like that). I am seeing very good mood and social behaviors in my son recently mostly thanks to new things we started recently (Bumetanide + Quercetine + FiberChoice Inulin + Flaxseed oil). If irritability is coming from gut, then Inulin is the answer, at least for us.

As far as your son is concerned, I think you gave a very good reason for his behaviors - higher than normal testosterone. Perhaps that is where you should focus. Things like Flaxseed, Reishi, and Spironolactone can be effective anti-androgens. Reishi has thousands of years of oriental medicine backing its effectiveness for calming. Spironolactone is used off label for anger. But you are already taking Bumetanide, so you have to consult a doctor because both are diuretics. Try FiberChoice Inulin. It is very easy to give. Tastes great!

As far as glutamate causing inflammation, it might be the other way around. Inflammatory cytokines like IFN trigger inflammation and high glutamate. I don't think that reducing glutamate would reduce inflammation. Fighting hidden viruses and inflammation is a good idea. An interesting thing about Reishi mushrooms is that not only they are very strong anti-androgens, but also boost immune system and inhibit viruses like Herpes. I haven't tried Reishi yet, but I will if behaviors become a problem.

Marya
Posts: 216
Joined: Tue Feb 21, 2017 4:14 pm

Re: Namenda response

Postby Marya » Sun May 28, 2017 3:14 am

Who tried Sarcosine or D-serine for NMDA receptors?

Marya
Posts: 216
Joined: Tue Feb 21, 2017 4:14 pm

Re: Namenda response

Postby Marya » Sun May 28, 2017 9:00 am

I was reading about NMDA receptors antagonist and I found that there some available out there, ketamine, methadone, memantine( which I think is Namenda), amantadine, and dextromethorphan.
Who has tried any of them except Namenda?

Have you considered alternative supplements like Sarcosine and D-serine?

However, NMDA receptors are associated to different neuro diseases, Autism, Alzheimer and Schizophrenia. I think from my understanding, whoever has that inactivation could run between these diseases, for example Autism in childhood then Shizophrenia in adulthood unless those receptors got addressed. Please correct me if I'm mistaken.
I do have this issue myself btw.

luis
Posts: 257
Joined: Thu Sep 25, 2008 8:42 pm

Re: Namenda response

Postby luis » Mon May 29, 2017 9:58 am

FatherOf2 wrote:
luis wrote:Thank you, Fo2.
Well, I'll have to study about this. It's new to me. It makes sense. Maybe it depends on the situation of the patient.
At this moment, I guess that my son needs more inhibition of NMDA receptors and more control of glutamate. (I read yesterday that some virus block the GAD enzyme, that is supposed to convert glutamate to GABA. And my son is definitely a virus boy.)

This is hard for me to understand. When my son takes supplements that increase glutamate, his speech increase a lot. But also his irritability and, on the limit, aggression. As you said, glutamate increases cognition. But it also increases inflammation.
Maybe what I need is to control virus better.

Thanks, again, Fo2.

We have very similar sons. My son too reacts very positively to glutamate boosting at first, but then irritability increases. Goldenseal does it for him. Whether my son's irritability is related to increased glutamate or something else remains to be answered. After all, Goldenseal has multiple actions, one of which is killing yeast. The fact that irritability from Goldenseal starts about 1 week after starting Goldenseal tells me that it might be related to changing gut flora (bad bacteria taking over small intestine, or something like that). I am seeing very good mood and social behaviors in my son recently mostly thanks to new things we started recently (Bumetanide + Quercetine + FiberChoice Inulin + Flaxseed oil). If irritability is coming from gut, then Inulin is the answer, at least for us.

As far as your son is concerned, I think you gave a very good reason for his behaviors - higher than normal testosterone. Perhaps that is where you should focus. Things like Flaxseed, Reishi, and Spironolactone can be effective anti-androgens. Reishi has thousands of years of oriental medicine backing its effectiveness for calming. Spironolactone is used off label for anger. But you are already taking Bumetanide, so you have to consult a doctor because both are diuretics. Try FiberChoice Inulin. It is very easy to give. Tastes great!

As far as glutamate causing inflammation, it might be the other way around. Inflammatory cytokines like IFN trigger inflammation and high glutamate. I don't think that reducing glutamate would reduce inflammation. Fighting hidden viruses and inflammation is a good idea. An interesting thing about Reishi mushrooms is that not only they are very strong anti-androgens, but also boost immune system and inhibit viruses like Herpes. I haven't tried Reishi yet, but I will if behaviors become a problem.


Thank you, Fo2. I'll search for Reishi. It seems interesting.
I'll come back later, with news.

Marya
Posts: 216
Joined: Tue Feb 21, 2017 4:14 pm

Re: Namenda response

Postby Marya » Mon May 29, 2017 9:09 pm

Marya wrote:I was reading about NMDA receptors antagonist and I found that there some available out there, ketamine, methadone, memantine( which I think is Namenda), amantadine, and dextromethorphan.
Who has tried any of them except Namenda?

Have you considered alternative supplements like Sarcosine and D-serine?

However, NMDA receptors are associated to different neuro diseases, Autism, Alzheimer and Schizophrenia. I think from my understanding, whoever has that inactivation could run between these diseases, for example Autism in childhood then Shizophrenia in adulthood unless those receptors got addressed. Please correct me if I'm mistaken.
I do have this issue myself btw.

Sorry I think I missunderstood this. Namenda is an inhibitor for NMDA so it is the opposite of Sarcosine.

FatherOf2
Posts: 1668
Joined: Mon Mar 11, 2013 1:37 am

Re: Namenda response

Postby FatherOf2 » Mon May 29, 2017 11:42 pm

Marya wrote:Sorry I think I missunderstood this. Namenda is an inhibitor for NMDA so it is the opposite of Sarcosine.

Yes, Namenda is opposite to sarcosine. Sarcosine, glycine, DMG and TMG will all potentiate NMDA receptors in the presence of glutamate. The action of sarcosine and glycine is confusing to me because I would expect an increased probability of seizures from their potentiation of NMDA receptors. Yet both are reported to reduce seizures:

https://www.ncbi.nlm.nih.gov/pubmed/20508295
... It is widely accepted that increased glutamatergic neurotransmission is involved in the initiation and propagation of seizures... However... the present findings indicate that sarcosine did not lower the seizure threshold. Conversely, sarcosine showed weak anticonvulsant properties by increasing the threshold current for the induction of tonic seizures. Therefore, sarcosine may be considered as a safe adjuvant treatment for schizophrenia without proconvulsant risk. In addition, the compound may serve as an interesting addition to epilepsy treatment.

http://www.nature.com/nrd/journal/v12/n11/box/nrd3893_BX2.html
... glycine has anti-epileptic effects in rodent models and it complements the suppression of seizures by GABA_A receptor agonists... The anti-epileptic effect of glycine is commonly attributed to an inhibitory regulation of neuronal excitability in the hippocampus through the activation of synaptic and extrasynaptic glycine receptors.

Article "More effective epilepsy treatment coming out of Israel": "The ineffectiveness of current epilepsy medication for a third of the population stems from problems associated with glycine, an amino acid which epileptic patients have a shortage of. Glycine, like other amino acids in the brain, serves as a neurotransmitter, either excitatory or inhibitory... Increasing its concentration in the brain has an antiepileptic effect. However, it is impossible to administer it to patients in its natural state, because it does not penetrate the blood-brain barrier that prevents medications from reaching their CNS target sites... The new CNS drug, valrocemide, is a combination of a known antiepileptic drug, valproic acid, and a glycine derivative, glycinamide."

If either Sarcosine or glycine raised probability of seizures, I would not be considering them because my son is taking anti-seizure meds to stabilize his EEG. Interestingly, Namenda can cause seizures at high doses even though it blocks NMDA receptors. In fact, patients with seizure disorder were excluded from the primary studies of Namenda. Namenda also induces neuronal lesions (vacuolation and necrosis) at 6 times the maximum recommended dose of 20 mg/day. Interestingly, glycine/sarcosine and Namenda, having different effects on NMDA receptors, are both touted to improve cognition. So, go figure this one.

Marya
Posts: 216
Joined: Tue Feb 21, 2017 4:14 pm

Re: Namenda response

Postby Marya » Tue May 30, 2017 7:35 am

FatherOf2 wrote:
Marya wrote:Sorry I think I missunderstood this. Namenda is an inhibitor for NMDA so it is the opposite of Sarcosine.

Yes, Namenda is opposite to sarcosine. Sarcosine, glycine, DMG and TMG will all potentiate NMDA receptors in the presence of glutamate. The action of sarcosine and glycine is confusing to me because I would expect an increased probability of seizures from their potentiation of NMDA receptors. Yet both are reported to reduce seizures:

https://www.ncbi.nlm.nih.gov/pubmed/20508295
... It is widely accepted that increased glutamatergic neurotransmission is involved in the initiation and propagation of seizures... However... the present findings indicate that sarcosine did not lower the seizure threshold. Conversely, sarcosine showed weak anticonvulsant properties by increasing the threshold current for the induction of tonic seizures. Therefore, sarcosine may be considered as a safe adjuvant treatment for schizophrenia without proconvulsant risk. In addition, the compound may serve as an interesting addition to epilepsy treatment.

http://www.nature.com/nrd/journal/v12/n11/box/nrd3893_BX2.html
... glycine has anti-epileptic effects in rodent models and it complements the suppression of seizures by GABA_A receptor agonists... The anti-epileptic effect of glycine is commonly attributed to an inhibitory regulation of neuronal excitability in the hippocampus through the activation of synaptic and extrasynaptic glycine receptors.

Article "More effective epilepsy treatment coming out of Israel": "The ineffectiveness of current epilepsy medication for a third of the population stems from problems associated with glycine, an amino acid which epileptic patients have a shortage of. Glycine, like other amino acids in the brain, serves as a neurotransmitter, either excitatory or inhibitory... Increasing its concentration in the brain has an antiepileptic effect. However, it is impossible to administer it to patients in its natural state, because it does not penetrate the blood-brain barrier that prevents medications from reaching their CNS target sites... The new CNS drug, valrocemide, is a combination of a known antiepileptic drug, valproic acid, and a glycine derivative, glycinamide."

If either Sarcosine or glycine raised probability of seizures, I would not be considering them because my son is taking anti-seizure meds to stabilize his EEG. Interestingly, Namenda can cause seizures at high doses even though it blocks NMDA receptors. In fact, patients with seizure disorder were excluded from the primary studies of Namenda. Namenda also induces neuronal lesions (vacuolation and necrosis) at 6 times the maximum recommended dose of 20 mg/day. Interestingly, glycine/sarcosine and Namenda, having different effects on NMDA receptors, are both touted to improve cognition. So, go figure this one.

Thank you fatherof2 for all this information. I would definitely do my research on this.
But if your son has inactivation of NMDA receptors, and you gave him Namenda, how did that work?

FatherOf2
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Re: Namenda response

Postby FatherOf2 » Tue May 30, 2017 9:20 am

Marya wrote:Thank you fatherof2 for all this information. I would definitely do my research on this.
But if your son has inactivation of NMDA receptors, and you gave him Namenda, how did that work?

At the time I gave him Namenda, I didn't know that my son had an inactivation of NMDA receptors. But even if I did know, I would have still tried Namenda because genetics are not the only determining factor of what inside.

Marya
Posts: 216
Joined: Tue Feb 21, 2017 4:14 pm

Re: Namenda response

Postby Marya » Tue May 30, 2017 12:46 pm

FatherOf2 wrote:
Marya wrote:Thank you fatherof2 for all this information. I would definitely do my research on this.
But if your son has inactivation of NMDA receptors, and you gave him Namenda, how did that work?

At the time I gave him Namenda, I didn't know that my son had an inactivation of NMDA receptors. But even if I did know, I would have still tried Namenda because genetics are not the only determining factor of what inside.

I see what you mean. It happened with me before when I was taking anything increase Dopamine I feel more aware and alert but with time I experience other symptoms like irritability, anxiety, mood swing and recently a mild panic attack! all of that because I didn't know that I have a high level of Dopamine and Adrenaline or at least I have that gene which could make Dopamine goes high very quickly.
I believe Namenda was fixing something but because of the inactivation of NMDA receptors the results wear off quickly. Please let us know when you start with Sarcosine.

Marya
Posts: 216
Joined: Tue Feb 21, 2017 4:14 pm

Re: Namenda response

Postby Marya » Mon Jun 19, 2017 10:02 pm

I have found this while I was reading on NMDA receptors;
The first evidence of a role for NMDA receptors in schizophrenia appeared in a manner very much like that for the dopamine hypothesis; through the observation of subjects given a chemical compound that altered normal NMDA signaling. When healthy volunteers were given a dose of ketamine (a drug that blocks NMDA receptor activity), they showed a wide variety of commonly seen schizophrenia symptoms (Begany 2004, Javitt and Coyle 2003). Besides replicating the psychotic positive symptoms, subjects showed a spectrum of negative symptoms, neurocognitive impairment, impaired eye-tracking, and neuronal potential abnormalities (these last two signs have been observed in schizophrenia patients during various studies). Further studies have shown that people with schizophrenia may have increased levels of a natural NMDA receptor antagonist (a chemical abbreviated as NAAG) in their prefrontal cortex, temporal cortex, and hippocampus (Begany 2004, Coyle and Tsai 2004).


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