As many become more aware to the glutamate connection to various health issues, glutamate blocker drugs are becoming more and more abundant.  What is the problem with this?  Here is my understanding of this…Some level of glutamate is necessary, but the problem is excess.  When you block glutamate, you’re blocking some of which is necessary, thus additional glutamate receptors are created as the body is scavaging for glutamate.  Increased glutamate receptors, means increased glutamate sensitivity. While REID focuses on lowering/balancing glutamate naturally, some have opted to use pharmaceutical options. Unfortunately in doing this, many have to continually increase their dose and/or have a hard time weening off of the medicine due to increased sensitivity to glutamate.  While I would not encourage the use of these drugs, here are a few that are more commonly used.  This list is not comprehensive. 

“There are many drugs that target your GABA receptors like Ativan, Xanax, Klonipin, Valium, and Neurontin (Gabapentin) and others. These drugs look similar in chemical structure as gamma-aminobutyric acid so they can fit in your GABA receptors, which artificially stimulates them, but they do not actually increase production. Therefore they do not address the underlying problem of not producing enough, because there must be some level of GABA present in order for these drugs to have an effect. Furthermore, anytime a substance is used to artificially stimulate a neurotransmitter the brain responds by reducing production or responsiveness, which results in more depletion of the neurotransmitter, which in this case is GABA. Therefore, any drugs that target GABA receptors or manipulates GABA or glutamate, will inhibit your ability to acquire and maintain balance.”

Amantadine- “Amantadine is an antiviral drug. The action against viruses is not entirely known. For treating other conditions in people (Parkinson’s disease), its effects are attributed to an increase in dopamine in the CNS. However it also is an N-methyl-D-aspartate (NMDA) receptor antagonist. As an NMDA antagonist, it will decrease tolerance to other analgesic drugs (e.g., opiates), but it probably does not possess many analgesic properties when used alone. There is only limited pharmacokinetic data available for animals”

Dextromethorphan- (commonly found in cough syrup & not necessarily REID approved)- Glutamate receptor antagonist. “Dextromethorphan (DM), a sigma receptor agonist and NMDA receptor antagonist, protects neurons from glutamate excitotoxicity, hypoxia and ischemia, and inhibits microglial activation”

Ibuprofen- Ibuprofen protects dopaminergic neurons against glutamate toxicity in vitro “Thus, NSAIDs protected neurons against glutamate excitotoxicity in vitro, and deserve further consideration as neuroprotective agents in Parkinson’s disease”

Low-dose naltrexone (LDN)– inhibits microglial activation “Low-dose naltrexone (LDN) has been demonstrated to reduce symptom severity in conditions such as fibromyalgia, Crohn’s disease, multiple sclerosis, and complex regional pain syndrome. We review the evidence that LDN may operate as a novel anti-inflammatory agent in the central nervous system, via action on microglial cells.”

Memantine (Namenda)– Is a glutamate blocker drug that has been used for those with Alzhimers but has recently gained popularity in the autism and PANS community.  Use of these glutamate blocker drugs do not come without risk.  Since some level of glutamate is necessary, blocking receptors triggers the body to create additional receptors.  The more receptors you have, the more sensitive you can become. Many find that they have to continually increase the dose and/or have problems coming off of the drugs. “Glutamate receptors are overactive, and N-methyl-D-aspartate (NMDA) receptor antagonists have therapeutic potential for the treatment of AD and other neurological disorders. Memantine is a noncompetitive NMDA antagonist that is considered a neuroprotective drug. Memantine’s capacity has been demonstrated in preclinical studies, and it is considered a useful symptomatic treatment for AD.”

Additionally, working to lower inflammation/glutamate by treating underlying sources inflammation (metals, microbial imbalances, parasites, microglial activation, poor detoxification pathways, various toxins, etc.) will also be hugely beneficial.  We’ve personally found homeopathy to be great for this.

The information shared within this blog has been gathered by a mother, not a physician, and should not act as medical advice. Under no circumstances shall I, or any contributors and affiliates of the blog, be responsible for damages arising from use of the blog.