It appears that glutamate is involved in migraine, dpression, and chronic degenerative brain diseases like parkinsons and alzheimers.
ONe of tHe leading drugs used in the treatment of alzheimers regulates Glutamate activity.

SO, how is it that we are putting boatloads of MSG in our foods?

— Begin quote from “dougiedd”

It appears that glutamate is involved in migraine, dpression, and chronic degenerative brain diseases like parkinsons and alzheimers.
ONe of tHe leading drugs used in the treatment of alzheimers regulates Glutamate activity.

— End quote

Have you got any evidence/references for this assertion?

You may find this recent thread on MSG illuminating: viewtopic.php?f=1&t=3638&start=0&hilit=msg

Evidence for what assertion?
That glutamic acid is likely involved in these diseases?

You could always remove all of it from your body and watch it turn into a great big blob of muck:

Hey Dougie,

I could only read the abstract of that article but it doesn’t mention migraine - is that contained within the full study?

If you want to avoid glutamate entirely you will struggle. It’s the most commonly occuring amino acid and is found in most ‘natural’ foods including meat, poultry, cheese, tomatoes, mushrooms and many other vegetables and even human breastmilk (which you should be able to avoid by now LOL).

MSG has been extensively studied for many years now and is considered ‘safe’ in the sense that it doesn’t “cause” any illness:

However, it can be a “trigger” for some migraineurs, just like any other trigger like nitrates or flickering lights or changes in barometric pressure.

This glutamate thing came up in the article posted by Silverpen where the author suggested MSG was a fertiliser for cancer. No glutamic acid and your entire nervous system grinds to a halt. We kinda need the stuff.

“Glutamic acid is the principal excitatory neurotransmitter in the mammalian central nervous system. Glutamic acid binds to a variety of excitatory amino acid receptors, which are ligand-gated ion channels. It is activation of these receptors that leads to depolarisation and neuronal excitation.”

Glutamate receptors, neurotoxicity and neurodegeneration.
Lau A, Tymianski M.

Division of Applied and Interventional Research, Toronto Western Research Institute, 399 Bathurst Street, Toronto, ON, Canada, M5T 2S8.

Glutamate excitotoxicity is a hypothesis that states excessive glutamate causes neuronal dysfunction and degeneration. As glutamate is a major excitatory neurotransmitter in the central nervous system (CNS), the implications of glutamate excitotoxicity are many and far-reaching. Acute CNS insults such as ischaemia and traumatic brain injury have traditionally been the focus of excitotoxicity research. However, glutamate excitotoxicity has also been linked to chronic neurodegenerative disorders such as amyotrophic lateral sclerosis, multiple sclerosis, Parkinson’s disease and others. Despite the continued research into the mechanisms of excitotoxicity, there are currently no pharmacological interventions capable of providing significant neuroprotection in the clinical setting of brain ischaemia or injury. This review addresses the current state of excitotoxic research, focusing on the structure and physiology of glutamate receptors; molecular mechanisms underlying excitotoxic cell death pathways and their interactions with each other; the evidence for glutamate excitotoxicity in acute neurologic diseases; laboratory and clinical attempts at modulating excitotoxicity; and emerging targets for excitotoxicity research.

Decreasing Brain Excitability with Migraine Therapy: Targeting Glutamate
(not rated)

By Andrew Charles, MD

Key Points:

    Uncontrolled brain activity may contribute to lack of migraine control.
    Glutamate, one of the most important brain pain chemicals causes increased brain activity.
    Blocking excessive brain activity without interfering with normal function could help control migraine.
    A drug, not currently approved for migraine, may decrease excess brain activity and control migraine.

Although multiple preventatives for migraine are currently available, many sufferers haven’t been able to find one that effectively reduces the frequency and severity of their migraine attacks. This may, at least in part, be due to excess brain activity, referred to as excitation, not adequately controlled by therapy. One promising area of research on new migraine treatments involves the chemical glutamate, one of the main neurotransmitters in the brain. A substance released by one nerve cell that allows it to communicate with another is a neurotransmitter. This communication or interaction occurs through a structure on the surface of the cell (or inside the cell), known as a receptor. Receptors selectively receive and lock onto specific substances, such as glutamate. Glutamate functions as an “excitatory” neurotransmitter, because when released it causes neighboring cells to become more active (excited).

Increasing evidence supports that excessive activation of cells in specific areas of the brain causes migraine. Special brain scans show that patients having migraine attacks may have waves of abnormal activity that spread across the surface of the brain (the cortex), as well as excitation of nerve centers deep within the brain (the brainstem). Both of these patterns of abnormal activity may involve the neurotransmitter glutamate.

Medications that stop glutamate nerve cell activity block waves of activity traveling across the brain surface in mice and rats that are very similar to those seen in migraine sufferers. Experimental studies also show glutamate receptors play a key role in the sensation of head pain, which occurs in brainstem nerve centers. These studies provide support for the use of glutamate receptor blockers for migraine therapy.

The challenge is to block excessive glutamate activity without interfering with normal cell function. Memantine (brand name in the is Namenda) may accomplish this. Memantine inhibits excessive activity of glutamate receptors, but does not have significant effects on the normal function of these receptors. In rodent experiments memantine blocks the waves of brain activity that may be a trigger for migraine.

Memantine is used for the treatment of Alzheimer’s disease and therefore available for migraine prevention only “off-label.” “Off-label” refers to the use of a medication for treatment of a condition that is different than the one for which it is FDA approved. Initial studies of the experiences of patients with memantine as a migraine preventive treatment are encouraging. Two preventative studies of memantine for migraine have been published – both showed promising results. Our group reviewed by survey the experience of patients with frequent migraine who had not had a satisfactory response to other therapies. 36 out of 54 treated with memantine for at least 2 months reported a significant reduction in estimated headache frequency, and improved function. Side effects were uncommon and generally mild. The most recently published study is an open-label study by Bigal, et al. In an open-label study both patient and practitioner know what the drug is being used. In 28 patients treated, monthly headache frequency was reduced from 21.8 days at baseline to 16.1 at 3 months. The mean number of days with severe pain was reduced from 7.8 to 3.2 at 3 months. However, neither study was the kind of formal clinical trial that is required to definitively prove that a treatment is effective. Such a trial is known as a randomized controlled trial (RCT). This kind of formal study is clearly needed in order to establish whether or not memantine can be widely recommended as a treatment for prevention of migraine. Two successful migraine RCTs are required in the for the FDA to consider labeling any drug as “indicated for migraine.” Until such time many insurance plans refuse coverage of such therapy “as not indicated,” but not all, given input from you and your practitioner. In the meantime, considering these issues and the early studies this may be a treatment worth discussing with your practitioner if other standard or conventional treatments have failed for prevention of migraine.

Memantine is generally very well tolerated — a minority of patients experience side effects that may include drowsiness, dizziness, or anxiety. Most, however, experience no adverse effects from the drug. At this time we do not know whether memantine will be proven to be effective in formal clinical trials and eventually approved for prevention of migraine. Regardless, however, initial laboratory and clinical studies indicate that targeting glutamate receptors represent a potential new approach to migraine therapy, and that this is an important topic for further investigation.

–Andrew Charles, M.D. Professor and Vice Chair, Director, Headache Research and Treatment Program, Department of Neurology, David Geffen School of Medicine at UCLA
December 2008


“The challenge is to block excessive glutamate activity without interfering with normal cell function.”

So what happens if you block the mechanism just a little bit too much? I have this image of someone freaking out with their limbs moving uncontrollably or not at all.

In the meantime, if you think your problems lie in overexposure to glutamate, eliminate it from your diet and let us know if you have found the holy grail.

Scott 8)

I dont think we can eliminate glutamate. BUt we can eliminate MSG.

Curious WHY MSG should be a trigger: science says it doesnt cross the blood brain barrier. Must do its work elsewhere in the body

— Begin quote from “dougiedd”

I dont think we can eliminate glutamate. BUt we can eliminate MSG.

— End quote

They are pretty much the same thing:

Is MSG different from glutamate?
The human body treats MSG the same as natural glutamate found in food. For instance, the body does not distinguish between free glutamate from tomatoes, cheese or mushrooms and the glutamate from MSG added to foods. Glutamate is glutamate, whether naturally present or from MSG.

If it’s a trigger for you - avoid tomoates, cheese and mushrooms as much as MSG. But you can’t avoid it all together if you want to, you know, live.

like heroin and natural endorphins are the same?

— Begin quote from “dougiedd”

like heroin and natural endorphins are the same?

— End quote

Bit of a stretch, however, if endorphins are a migraine trigger for you then to be on the safe side, definitely avoid heroin. And ultra marathons. :lol:

Personally I think heroin and MSG are in the exact same ballpark. Being caught with MSG should result in the death penalty just like heroin should you happen to have a bag of it while touring Singapore.

as far as I know heroin and msg are not at all the same

I’ve been dealing MSG for years now…it’s a little known black market. Gotta pay for my MAV meds :lol:



I hear on the street junkies have been turning MSG into a cheaper rock – an MSG crack. The could call it Mack.