posted
I am in my second month of treatment. I showed my LLMD all of the vitamins I am taking as well as yeast and bacterial supports. I showed him a product called MAXGXL. He liked it and thought it was a good product. Has anyone taken this. Several of my friends do (non lyme) with good results. It has:
Vitamim C 250 mg L-Glutamine 750 mg N-Acetyl Cysteine (he really liked this) 375 mg 488 mg combo including Glucosamine, Milk thistle extract and silmarin
Thanks for any input
Posts: 749 | From State full of ticks | Registered: Dec 2008
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posted
We have no experience with this product. But, it seems like it has great ingredients and it does sound like it is a good supplemental support. And, if your LLMD is in favor of it then that is terrific!
Do you feel that it is helping/do you feel any difference yet? Not that it means anything- nutritional support takes time... but sometimes if you compare where you were with where you are now, you can kind of tell if it's helping. But I realize that you mentioned it hasn't been long...
Hope you are having a good day today!
Posts: 89 | From NC | Registered: Jun 2008
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Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
- L-Glutamine 750 mg
I don't think lyme patients should be supplementing with L-Glutamine - except in very small amounts only for stomach repair and if DGL and slippery elm were first tried.
Glutamate neurotoxicity is much more likely for lyme patients.
L-Glutamine can help with the stomach lining but be careful if anxiety or central nervous system irritation occur. Anyone with a seizure disorder should avoid this (as as sole supplement), unless in small amounts as part of a balanced formula.
Glutamine can convert to glutamic acid in the brain and that can create further toxicity & irritation to brain/nerve cells for those with neurological illness and a compromised blood brain barrier (as with lyme):
AMINO ACID SUPPLEMENTS I: GLUTAMINE - with Reference to the Related Compound Glutamate
-by Subhuti Dharmananda, Ph.D.
Excerpt, half way down the article:
. . . Glutamate in Neurological Diseases
The other concern about glutamate is related to its essential role as a neurotransmitter. The levels of glutamate in the central nervous system (brain and spinal cord) are highly regulated, since the neurons have sensitive receptors for the compound.
* In some neurological diseases, it is found that glutamate levels in the central nervous system become unusually high at sites of pathology. This can occur, for example, if the rate of degradation of glutamate is slowed by an impairment of the enzymes that are involved.
* Also, glutamate is excreted by immune cells that take part in inflammatory processes; the result is high local concentrations at the neurons in progressive neurological diseases such as MS and ALS.
* Glutamate levels in the central nervous system can also increase when the blood brain barrier is substantially weakened, as occurs after neurological surgery.
* The excess glutamate at the neuron acts as a poison; at high enough levels, the nerves exposed to glutamate can be completely and permanently damaged, so that they are no longer capable of transmitting signals.
* Thus, while glutamate is a major component of the body, and an essential part of the nervous system, high levels localized in the nerve cells can be quite toxic, and this is readily demonstrated in animal models.
* Laboratory research has revealed that in the progressive, debilitating disease ALS, one of the many processes involved in disease progression appears to be damage of nerve cells by accumulation of glutamate.
* In relation to multiple sclerosis, changes in control of glutamate homeostasis in the central nervous system might contribute to demyelination of the white matter of the brain (19).
Based on preliminary animal studies, it has been suggested that glutamate dumped by immune cells can exacerbate the nerve damage (20).
* One of the means by which a stroke (causing blockage of blood circulation to the brain) results in brain damage is through an increase in glutamate levels in the brain cells (of course, oxygen deprivation and other effects are also contributors). These findings point to local glutamate excess as an important factor in brain diseases.
* Since glutamine is converted to glutamate, supplementing glutamine at very high levels in persons who have such neurological disorders may be contraindicated.
. . . . - Full article at link above. -
- If someone has a reaction to L-Glutamine, this is of interest as it addresses glutamate neurotoxicity: ----------------------
Prevention of ammonia and glutamate neurotoxicity by carnitine: molecular mechanisms.
Llansola M, Erceg S, Hernandez-Viadel M, Felipo V.
Laboratory of Neurobiology, Instituto de Investigaciones Citologicas, FVIB, Valencia, Spain.
Carnitine has beneficial effects in different pathologies and prevents acute ammonia toxicity (ammonia-induced death of animals).
Acute ammonia toxicity is mediated by excessive activation of the NMDA-type of glutamate receptors, which mediates glutamate neurotoxicity.
We showed that carnitine prevents glutamate neurotoxicity in primary cultures of cerebellar neurons. This supports the idea that the protective effect of carnitine against ammonia toxicity is due to the protective effect against glutamate neurotoxicity.
We are studying the mechanism by which carnitine protects against glutamate neurotoxicity. Carnitine increases the binding affinity of glutamate for metabotropic glutamate receptors. The protective effect of carnitine is lost if metabotropic glutamate receptors are blocked with specific antagonists.
Moreover, activation of metabotropic glutamate receptors by specific agonists also prevents glutamate neurotoxicity.
This indicates that the protective effect of carnitine against glutamate neurotoxicity is mediated by activation of metabotropic glutamate receptors. The molecule of carnitine has a trimethylamine group.
Different compounds containing a trimethylamine group (carbachol, betaine, etc.) also prevent ammonia-induced animal death and glutamate-induced neuronal death.
Moreover, metabotropic glutamate receptor antagonists also prevent the protective effect of most of these compounds. We summarize here some studies aimed to identify the mechanism and the molecular target that are responsible for the protective effect of carnitine against ammonia and glutamate neurotoxicity.
Finally it is also shown that carnitine inhibits the hydrolysis of inositol phospholipids induced by activation of different types of metabotropic receptors, but this effect seems not responsible for its protective effects.
PMID: 12602515 [PubMed - indexed for MEDLINE] -
Posts: 48021 | From Tree House | Registered: Jul 2007
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Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
- As glucosamine is a frequently suggested supplement for arthritis . . .
and (according to the authors below) N-acetylglucosamine is contraindicated with lyme, I'd want to know more about glucosamine in general regarding action around spirochetes. --------------
BIOCHEMISTRY OF LYME DISEASE: BORRELIA BURGDORFERI SPIROCHETE / CYST
Excerpt:
. . . A popular treatment for arthritis includes the administration of chondroitin sulfate and N-acetylglucosamine.
If the arthritis is Lyme-induced, N-acetylglucosamine is contraindicated. 22 (See Chart 14.) -
Posts: 48021 | From Tree House | Registered: Jul 2007
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