Do we all believe this theory that excessive glutamate is the primary villain with visual snow?

I genuinely do not know, but I hear this theory a lot regarding visual snow and it being the cause.

IF (and this is a big if) this is true. Then it would be safe to say that there is “damage” brain cells due to an excessive amount of glutamate in the brain. In other words there is neuronal death.

Excitotoxicity has been linked/involved in many disease (such as Epilepsy, Parkinson’s , RLS, Hyperactivity and anxiety disorders).

In terms of visual snow syndrome. There are a slew of symptoms associated with visual snow. Such as brain fog, dpdr, tinnitus and so fourth.

Causes of excitotoxicity (that ultimately causes visual snow) is:

-severe stress -sleep apnea -head trauma -mold exposure -Lyme disease -Narcolepsy -Free radicals

I am currently taking Low-Dose Naltrexone, as a possible way to treat excitotoxity. The potential reason for visual snow syndrome.

There have been trials that have shown to reduce excitotoxity and microglial activation (an inflammatory response).

It has also been show to Down regulate inflammatory cytokines. As well as reducing inflammation and oxidative stress.

Please let me know when you guys think of the treatment that I’m doing. Please do your research and look up low-dose naltrexone.

Title pretty much says it all, but since I need to fill the description, I'll explain why I care. I drink extremely large amounts of green tea (at least 5 cups a day), and although I know there's not nearly enough l-theanine in that amount of green tea to cause side effects (in most people), I'm curious as to what the literature says about this.

I was taking a pharmaceutical NMDA/AMPA antagonist called topiramate AKA Dopamax/Topamax. It is notorious for making people stupid. Added to which I stopped it cold turkey.

Its symptoms include a sort of brain slowing and disruption similar to pseudo-ADHD, loss of words, loss of memory (confusion when waking up - not knowing where I live), inability to learn new things (maybe linked to long term potentiation), and of course depersonalization which is common with NMDA antagonists.

I don't know much about this stuff, but I'm looking for suggestions?

So far I have read about the TCA opioid Tianeptine helping regulate glutamate

Also, sarcosine might help upregulate NMDArs at the glycine site.

There's also nefiracetam - although it may well be toxic to the kidneys and more importantly the precious testes.

That's it. Any insight? I'd really appreciate it. I'm brain dead.

I have tried:

Noopept, NAC, aniracetam, oxiracetam, colouracetam, fasoracetam, lions mane, bacopa moneri, ginko, rhodolia rosea, sulbutiamine, b12, p-5-p, VD+VK2, LD Naltrexone, selegiline at both MAO-B and nonselective MAOI doses, modafinil for glutmate regulation.

GABA analogs like pregabalin now seem to ease depersonalization and actually increase verbal fluency.

There's also semax/selank for more BDNF, and also NSI-189 - but that could do anything, it's proven safe short term, but who knows what it activates something that causes tumours to grow 10 years from now.

I'd be grateful for any thoughts at all.

Edit: been of it for a year.

Hi, I suspect I have excitotoxicity and many other neurological issues from heavy metal toxicity/and/or brain trauma.

Would memantine be any helpful for excitotoxicity? What's your experience with it? I know that ketamine is a great NDMA receptor antagonist and it helps with it, I have also tried it before and indeed I felt so much better on ketamine, I can't access it anymore though.

During some mma training I got knocked out heavily, losing consciousness for 10-20 seconds. I have been dizzy for the whole day, and then maybe a week after I had 1-2 days of completele memory blackout, but that was during some party and I just think I drank some spiked up drink by a mistake from someone random. Yet I'm still so unsure about any of that, I haven't done any brain examination or anything like that. All I know is during that time I have had some dental procedures done (possibly amalgams used) and some tattoos done as well. My theory is that they caused heavy metal toxicity and I have indeed been suffering with chronic health issues since that time. I thought it was just SIBO at first, then mold toxicity, then some autoimmune disease, now I'm even more sure about heavy metal toxicity causing all of this probably from amalgams. I've read excitotoxicity is connected to heavy metal toxicity. But it's still somewhere in my head, I'm wondering if I actually had brain trauma and if it could have caused some of the issues I've been experiencing. My issues are - achy joints, muscles, muscle wasting, bones prone to injury, light sensitivity, dry eyes (sjogrens syndrome symptoms), memory and concentration problems, neuropathy, fibromyalgia, sibo, dehydration and many more. I'm better when I exercise but different diets dont work on me, I've tried carnivore, paleo, keto, vegan, and I honestly do better eating a normal diet or fast food diet.

Anyone can relate maybe and want to share their experiences? I'm interested in hearing other opinions!

7,8-Dihydroxyflavone (tropoflavin) protects against excitotoxicity in amphetamine and dopaminergic neurotoxicity in methamphetamine.

Someone please explain this theory (that is is the cause for visual snow).

I have severe brain fog and have had terrible brain fog for a year going on 2. It all happened acutely. In a matter of seconds. The fog, the snow, it’s been bad and just want it to go away.

Can someone please explain this theory, I would greatly appreciate it.

I have read many articles that state ALS is from Excitotoxicity brought on by an excess of Glutamate in the brain. I find this interesting because there are food products that can increase Glutamate in the brain. Recently I read that an high dose of THC can also lead to Glutamate Excitotoxicity. I thought THC slowed down progresstion of ALS? Could it be possible that someone taking medication like anxiety pills and high dose of THC can actually give themselves ALS? The reason I am asking is because with the current state of mental health (anxiety medication) and the legalization of Marijuana (high does) could this lead down a bad path mixing the two?

Hey guys, quick question. I was taking 30 grams of l-glutamine powder for 3 weeks to heal some gut issues and at the 3 week mark I was hit hard with anxiety, a couple of nights of insomnia, some slight tinnitus and ear clogged feeling at times, and just general over worry. I was in a pretty heavy calorie deficit with low carbs. So I’m thinking my serotonin and hormone levels were prob low as well and played a part in this…

From what I’m reading it looks like I built up too much glutamate and threw off my glutamate/gaba balance. It’s been about a week since I cut out the glutamine and I’m feeling MUCH better, but still have some low level anxiety and my left ear just feels like it has a small amount of pressure at times. I’m sure it will slowly all come back to baseline.

My question is do you think this was glutamate excitotoxicity? And have I possibly damaged my brain here? Or is this goofy anxiety just playing with my mind and needless worry?

Thanks guys!

Ketamine, at sub-anesthetic doses, acts as a NDMA receptor antagonist, which blocks glutamate receptors and can potentially act as a neuroprotective agent in cases of excitotoxicity due to excess glutamate. However, it also releases a glutamate surge at the same time. What I’m wondering is, can ketamine usage, in a therapeutic setting, lead to glutamate toxicity, or does it in fact have the opposite effect? Case in point, I am receiving ketamine infusions for depression. It’s working wonderfully. However, directly following my second infusion, I immediately noticed neuropathic muscular pain, hyperalgesia, allodynia, etc. I know ketamine treatments for pain are supposed to have the total opposite effect, which is why this is so puzzling. My concern is that the hyperglutamergic state could have had this effect on my body, as excitotoxicity/excess glutamate is said to cause these symptoms. I could have literally just suddenly developed this for any reason, but I am curious, because I see various answers everywhere. Is this a possibility or was what happened to me a coincidence? Note: not asking for medical advice, just wondering about the mechanism of action.

Just been listening to the hoffmann labs podcast and he mentioned creatine in his episode on depression. Creatine interacts with the NMDA system in some way and, lo and behold, google shows a lot of papers that mention how it prevents excitotoxicity induced by MK-801, a dissociative drug. Now I'm not really sure about in what ways dissociative use is damaging the brain at all but have a vague memory of hearing that after the effects wane there is an over-excitement of the glutamatergic system as a sort of rebound? Would creatine be a useful addition to the dissociative lover's diet?

But on the other hand, I also remember creatine in the context of possible kidney damage. Should kreatine and arylcyclohexylamines maybe not be taken within a certain time frame of each other to avoid damage? Should people taking it for sports-related benefits be cautious about dissociative use?

(also: the stupid automod seems to be a little too proactive regarding "low effort" titles and deleting posts, hrmphf...)

People quitting benzos are naturally worried about seizures and neuronal damage during withdrawal. This is a quick guide on what's going on with seizures and what can be done very practically, besides tapering slowly, to prevent damage and seizures. Proceed implementing this with caution and judgment. Specifically, do not load up on strong nmda antagonists.[edit: I'm advocating use for short term.]Ask your physician if possible.

Quick and crude overview of mechanisms: Gaba is the main inhibitory neurotransmitter. Glutamate is the main excitatory neurotransmitter. They counteract each other the way the gas and break on a car do. Benzo addiction is like pressing the break and having the hand break on so your body upregulates glutamate, presses the gas. But if you stop taking benzos your neurons will be in over acceleration mode which can lead to seizures and excitotoxicity. Excitotoxicity -- glutamate binds to ampa and nmda receptors and allow in too much calcium which results in oxidative stress and to cell damage (ROS leading to inflammation and cell membrane damage)

NMDA antagonists to the rescue: NMDA antagonists should be protective against seizures and excitotoxicity by inhibiting the calcium channels. This lets go of the gas in a time when your breaks are cut (gaba withdrawal).

https://pubmed.ncbi.nlm.nih.gov/9593834/

On NMDA and Excitotoxicity: https://pubmed.ncbi.nlm.nih.gov/10920427/

Nmda antagonists and sensitization.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5766724/

" It is well known that agonists of NMDA or AMPA receptors can elicit seizures in animal or human subjects, while antagonists have been shown to inhibit seizures in animal models, suggesting a potential role for NMDA and AMPA receptor antagonists in anti-seizure drug development." https://www.mdpi.com/2218-273X/10/3/464/pdf#:~:text=It%20is%20well%20known%20that,in%20anti%2Dseizure%20drug%20development.

NMDA antagonists that are accessible without having to wait in case you just read this and you want to act: magnesium and DXM and relates compounds (found in NYQuil and other cough medicines). https://jnnp.bmj.com/content/jnnp/57/3/333.full.pdf Although abuse of DXM can lea

Can someone explain glutamate excitotoxicity and why it occurs like I'm a 5 year old with 2 braincells?

Hello all,

After some reading on the subject, i understand excitotoxicity and the consequential neuronal damage as follows;

• Excessive release of excitatory glutamate that is not 'counterbalanced' by GABA-activity overstimulates glutamate receptors (NMDA, kainate, AMPA).
• This leads to excessive influx of calcium into the cell, causing it to become overexcited and starting a process during which the cell is damaged or dies.

3 questions, any input on either one of them is greatly appreciated;

• The use of NMDA antagonists is widely suggested as a means to minimize the damage by excitotoxicity. Conversely, i've seen it suggested that by antagonising the NMDA-receptors, the excess glutamate will essentially flock towards the kainate and AMPA- receptors, again causing excitotoxicity.
• I've read multiple articles suggesting that Nifedipine and nimodipine, calcium channel antagonists, might exacerbate cell death in an excitotoxic environment, despite them limiting the excessive calcium influx by blocking the calcium channels. How does this work?
• I've read multiple studies that suggested the use of potassium channel openers to 'hyperpolarize' the cell and reduce its excitability, to reduce the risk of overexcitation and excitotoxicity. However, an excessive efflux of potassium might again exacerbate toxicity? Can someone clarify this process?

Should anyone have any knowledge on either directly lowering glutamate or attenuating excitotoxicity through other mechanism, please feel free to share. Thank you all for taking the time to read my question and share your knowledge.

Regards

Considering how many substances we all put into our bodies I was thinking about if things like excess glutamate or other transmitters are leaving our brain cells worse off than if we were to just perform at baseline. Just a thought

I presume that tapering is like a reigning in of a biological system gradually that could otherwise potentially be damaged by a large swing in its activity. For example, If glutamergic activity had been suppressed by increased GABA inhibition, the worse and more sudden the rebound, the worse the resultant excitotoxicity, is that correct?

The anxiety felt during the hangover I assume has to do with GABA activity being lower, are gaba and glutamate activity counter to each other in the system like a seesaw or is this too much of an oversimplification?

Could someone point me to informative talks or videos about alcohol’s pharmacological action?

Glutamate receptors and their roles are very complex, but my understanding is that one property of NMDA receptor antagonism is protection against excitotoxicity in some circumstances.

As NMDA receptor antagonism seems to be a fairly common mechanism of action for some nootropics (e.g. memantine and agmatine) and other commonly used drugs (Ketamine, DXM) and supplements (Magnesium), I am curious if there is any potential or evidence for increased excitotoxicity following withdrawal of NMDA receptor antagonists, particularly after extended use, maybe due to some sort of glutamate/glutamate receptor dysregulation.

I know there is a lot of pharmacodynamic variability between the various antagonists so I'm sure it's not a clear cut situation, but I'm just curious if anyone here knows anything about this subject.

I know that the chief inhibitory system in the human body is the GABA system. This certainly explains the withdrawals we get from drugs that target the GABA receptors (as GABA basics acts more like the brakes in a car).

Would NMDA antagonist ms (specifically memantine) cause rebound excitation/excitotoxicity upon discontinuation? I only found few cases reported in literature but they were of older individuals that had preexisting neurodegenerative conditions that may very well have contributed to their symptoms.

Since memantine antagonizes the NMDA receptors blocking glutamate from binding, wouldn’t that results in upregulation and subsequent symptoms similar to or dangerous like benzo withdrawals?

So, if you do too much NMDA antagonists can the withdrawal become excitotoxicity? Because ethanol withdrawal is more complicated than benzos/barbs withdrawal - maybe is due to glutamate excesse along with gaba depletion. It's something dangerous? What about the symptoms?

As the title states, I've been trying to think about how to reduce the excitotoxicity from my stimulants. I have been trying things out, but feel unsure now...

 

Magnesium Glycinate

I've read about the role of NDMA receptors in this, and have been taking Magnesium Glycinate... but, upon reading a bit more myself from the wikipedia I feel uncertain. Specifically:

"Excitotoxicity is implied to be involved in some neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and Huntington's disease. Blocking of NMDA receptors could therefore, in theory, be useful in treating such diseases.It is, however, important to preserve physiological NMDA receptor activity while trying to block its excessive, excitotoxic activity. This can possibly be achieved by uncompetitive antagonists, blocking the receptors ion channel when excessively open"

"Excitotoxicity has been thought to play a role in the degenerative properties of neurodegenerative conditions since the late 1950s. NMDA receptors seem to play an important role in many of these degenerative diseases affecting the brain. Most notably excitotoxic events involving NMDA receptors have been linked to Alzheimer's disease and Huntington's disease as well as with other medical conditions such as strokes and epilepsy. Treating these conditions with one of the many known NMDA receptor antagonists, however, lead to a variety of unwanted side effects, some of which can be quite severe. These side effects are, in part, observed because the NMDA receptors do not just signal for cell death but also play an important role in its vitality. Treatment for these conditions might be found in blocking NDMA receptors not found at the synapse"

From there, I'm not exactly sure what to think about my Magnesium Glycinate supplement, and if I am supposed to take 400mg before, at the same time, or after I take my stimulant? Should I be taking this at night as well, before bed?

 

Ubiquinol and PQQ:

I'd read a lot about how ubiquinol is so beneficial for the heart, blood pressure, energy levels, and even provides antioxidant qualities. I began supplement with Jarrow's QH-+PQ, and love it. However, I've become uncertain about how much I should be taking daily... before, at the same time, or after my stimulant usage? I read that it may be used more

Hi all,

I'm currently going through a slowly tapered withdrawal from 1,5 mgs xanax daily, doctor prescribed. Looking for any supplements that might help my body and brain deal with the toxicity during withdrawal. Currently on omega 3 fishoil, l-theanine, melatonin, magnesium and zinc. Any further input is highly appreciated.

Was considering Taurine, any experiences with that?

Thank you all

Hi all,

Was wondering if any of you could shed some light on the relation between potassium channel openers and excitotoxicity.

The following studies suggest that potassium channel openers could prevent neuronal damage through various mechanisms, including indirect antagonism of the NMDA-receptor through activation of the K+ channels.

• http://www.heraldopenaccess.us/fulltext/Addiction-&-Addictive-Disorders/Neuronal-Potassium-Channel-Openers-Flupirtine-(SNEPCO)-in-the-Treatment-of-the-Alcohol-Withdrawal-without-Psychiatric-Comorbidity.pdf
• https://onlinelibrary.wiley.com/doi/full/10.1046/j.1471-4159.1997.69041570.x?fbclid=IwAR16GmXmQcb3ld0-1c-abGZr0vIoGdQKSmSnlrNNduiG9GrF0Enyn05UTY8
• https://www.sciencedirect.com/science/article/abs/pii/030439409090454H

However, i've seen it suggested plenty of times that opening the potassium channels could greatly exacerbate cell death in the case of overexcitation.

Could any of you explain in more detail how this process works, and what adverse consequences might be overlooked by these studies/how potassium channel openers could contribute to cell death during benzo withdrawal?

Thank you all!

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1865572/pdf/nihms18758.pdf

KETONES INHIBIT MITOCHONDRIAL PRODUCTION OF REACTIVE OXYGEN SPECIES PRODUCTION FOLLOWING GLUTAMATE EXCITOTOXICITY BY INCREASING NADH OXIDATION

Marwan Maalouf1,

Patrick G. Sullivan2,

Laurie Davis2,

Do Young Kim1,

and Jong M. Rho1

1 Barrow Neurological Institute and St. Joseph's Hospital & Medical Center, Phoenix, Arizona, 85013, United States 2 Spinal Cord and Brain Injury Research Center, Department of Anatomy & Neurobiology, University of Kentucky, Lexington, Kentucky 40536, United States

Abstract

Dietary protocols that increase serum levels of ketones, such as calorie restriction and the ketogenic diet, offer robust protection against a multitude of acute and chronic neurological diseases. The underlying mechanisms, however, remain unclear. Previous studies have suggested that the ketogenic diet may reduce free radical levels in the brain. Thus, one possibility is that ketones may mediate neuroprotection through antioxidant activity. In the present study, we examined the effects of the ketones β-hydroxybutyrate and acetoacetate on acutely dissociated rat neocortical neurons subjected to glutamate excitotoxicity using cellular electrophysiological and single-cell fluorescence imaging techniques. Further, we explored the effects of ketones on acutely isolated mitochondria exposed to high levels of calcium. A combination of β-hydroxybutyrate and acetoacetate (1 mM each) decreased neuronal death and prevented changes in neuronal membrane properties induced by 10 μM glutamate. Ketones also significantly decreased mitochondrial production of reactive oxygen species and the associated excitotoxic changes by increasing NADH oxidation in the mitochondrial respiratory chain, but did not affect levels of the endogenous antioxidant glutathione. In conclusion, we demonstrate that ketones reduce glutamate-induced free radical formation by increasing the NAD+/NADH ratio and enhancing mitochondrial respiration in neocortical neurons. This mechanism may, in part, contribute to the neuroprotective activity of ketones by restoring normal bioenergetic function in the face of oxidative stress.

Keywords glutamate; neurotoxicity; diet; mitochondria; oxidation; stress

DISCUSSION

The principal finding of our study is that ketones, produced by the liver under conditions of fasting, calorie restr

I have read many articles that states ALS is from Excitotoxicity brought on by an excess of Glutamate in the brain. I find this interesting because there are food products that can increase Glutamate in the brain. Recently I read that an high dose of THC can also lead to Glutamate Excitotoxicity. I thought THC slowed down progresstion of ALS? Could it be possible that someone taking medication like anxiety pills and high dose of THC can actually give themselves ALS? The reason I am asking is because with the current state of mental health (stress) and the legalization of Marijuana could this lead down a bad path.

I have read many articles that states ALS is from Excitotoxicity brought on by an excess of Glutamate in the brain. I find this interesting because there are food products that can increase Glutamate in the brain. Recently I read that an high dose of THC can also lead to Glutamate Excitotoxicity. I thought THC slowed down progresstion of ALS? Could it be possible that someone taking medication like anxiety pills and high dose of THC can actually give themselves ALS? The reason I am asking is because with the current state of mental health (anxiety medication) and the legalization of Marijuana (high does) could this lead down a bad path mixing the two?

I have read many articles that states ALS is from Excitotoxicity brought on by an excess of Glutamate in the brain. I find this interesting because there are food products that can increase Glutamate in the brain. Recently I read that an high dose of THC can also lead to Glutamate Excitotoxicity. I thought THC slowed down progresstion of ALS? Could it be possible that someone taking medication like anxiety pills and high dose of THC can actually give themselves ALS? The reason I am asking is because with the current state of mental health (stress/medication ) and the legalization of Marijuana could this lead down a bad path.

Hello all,

After some reading on the subject, i understand excitotoxicity and the consequential neuronal damage as follows;

• Excessive release of excitatory glutamate that is not 'counterbalanced' by GABA-activity overstimulates glutamate receptors (NMDA, kainate, AMPA).
• This leads to excessive influx of calcium into the cell, causing it to become overexcited and starting a process during which the cell is damaged or dies.

3 questions, any input on either one of them is greatly appreciated;

• The use of NMDA antagonists is widely suggested as a means to minimize the damage by excitotoxicity. Conversely, i've seen it suggested that by antagonising the NMDA-receptors, the excess glutamate will essentially flock towards the kainate and AMPA- receptors, again causing excitotoxicity.
• I've read multiple articles suggesting that Nifedipine and nimodipine, calcium channel antagonists, might exacerbate cell death in an excitotoxic environment, despite them limiting the excessive calcium influx by blocking the calcium channels. How does this work?
• I've read multiple studies that suggested the use of potassium channel openers to 'hyperpolarize' the cell and reduce its excitability, to reduce the risk of overexcitation and excitotoxicity. However, an excessive efflux of potassium might again exacerbate toxicity? Can someone clarify this process?

Should anyone have any knowledge on either directly lowering glutamate or attenuating excitotoxicity through other mechanism, please feel free to share. Thank you all for taking the time to read my question and share your knowledge.

Regards

Hello all,

After some reading on the subject, i understand excitotoxicity and the consequential neuronal damage as follows;

• Excessive release of excitatory glutamate that is not 'counterbalanced' by GABA-activity overstimulates glutamate receptors (NMDA, kainate, AMPA).
• This leads to excessive influx of calcium into the cell, causing it to become overexcited and starting a process during which the cell is damaged or dies.

3 questions, any input on either one of them is greatly appreciated;

• The use of NMDA antagonists is widely suggested as a means to minimize the damage by excitotoxicity. Conversely, i've seen it suggested that by antagonising the NMDA-receptors, the excess glutamate will essentially flock towards the kainate and AMPA- receptors, again causing excitotoxicity.
• I've read multiple articles suggesting that Nifedipine and nimodipine, calcium channel antagonists, might exacerbate cell death in an excitotoxic environment, despite them limiting the excessive calcium influx by blocking the calcium channels. How does this work?
• I've read multiple studies that suggested the use of potassium channel openers to 'hyperpolarize' the cell and reduce its excitability, to reduce the risk of overexcitation and excitotoxicity. However, an excessive efflux of potassium might again exacerbate toxicity? Can someone clarify this process?

Should anyone have any knowledge on either directly lowering glutamate or attenuating excitotoxicity through other mechanism, please feel free to share. Thank you all for taking the time to read my question and share your knowledge.

Regards