Molecules symptoms and conditions

I am re-posting this from June. I believe that we have many reasons to suspect that Singulair does indeed penetrate the blood brain barrier. I personally believe that under certain unusual conditions that Singulair can cause neurological damage. I tried before to put together a scenario of brain biochemistry that could explain how this can happen. Of course, I am just hypothesizing and all of my ideas will not prove to be totally correct. From the number of postings here regarding neurological symptoms, I believe that there is an answer out there somewhere. Why the FDA is not searching for this answer is a complete mystery to me.

I believe that it is possible that Singulair causes the same biochemical response in the brain that is cited in this study -- thus causing neurological damage.

"Thus, elevated NO production leading to mitochondrial dysfunction, glutamate release, and excitotoxicity may contribute to neuronal death in neurological diseases."

IS SINGULAIR CAUSING THE DEATH OF NERVE CELLS IN SOME PATIENTS? DOES THIS HAPPEN - ALTHOUGH INFREQUENTLY- BECAUSE OF GENETIC OR BIOCHEMICAL FACTORS OR BOTH?

June 12th
2008
2:56 AM
I have stated many times that I am not an expert. I just post what I find. This has been a mind boggling journey for me. This is way over my head but I struggle to read and understand. Finding answers to why children are suffering from neuro-psychiatric side effects is worth the effort.

I have made the following observations.

1. Some quinolines are known to be able to cross the blood brain barrier.
2. Molecules that ionize are known to be more likely to be able to cross cell membranes. So if montelukast ionizes as a result of change in blood pH to sufficient acid conditions, then it could be possible that it does in fact cross the blood brain barrier.
3. We know that there are cysLT1 receptors in the brain.
4. We know that researchers believe that montelukast may bind at the arginine of the cysLT1 receptor.
5. We know that arginine contains four nitrogens. And montelukast contains one.
6. We don't know what happens to those nitrogens. Are those nitrogens converted to nitric oxide?
7. We do know what macrophages create nitric oxide as I posted.
8. We do know that if something cause excessive nitric oxide to build in the brain that there would be damage to the neurons.

Some people may remember when I got stuck at the astrocytes, the cysLT1 receptors and glutamate. I keep looking for research reports that may shed more light on this.

Titre du document / Document title
Nitric oxide causes glutamate release from brain synaptosomes
Auteur(s) / Author(s)
MCNAUGHT K. S. P. (1) ; BROWN G. C. (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Biochemistry, University of Cambridge, Cambridge, ROYAUME-UNI
Résumé / Abstract
We determined the ability of pathological levels of nitric oxide (NO) to cause glutamate release from isolated rat brain nerve terminals using a fluorometric assay. It was found that NO (0.7 and 2 μM) produced (4 and 10 nmol/mg of synaptosomal protein) Ca2+-independent glutamate release from synaptosomes (after 1 min of exposure). Spermine/NO complex (spermine NONOate; a slow NO donor) and potassium cyanide (an inhibitor of cytochrome oxidase) also caused Ca2+-independent glutamate release. Preincubation of synaptosomes with 5 μM 1H- oxadiazole quinoxalin-1-one (an inhibitor of soluble guanylyl cyclase) had no effect on NO-induced Ca2+-independent glutamate release. Ca2+-independent glutamate release produced by NO was greater in a low-oxygen medium. NO, spermine NONOate, and potassium cyanide inhibited synaptosomal respiration with a similar order of potency with respect to their ability to cause glutamate release. Because NO has been shown previously to inhibit reversibly cytochrome oxidase in competition with oxygen, our findings in this study suggest that NO (and cyanide) causes glutamate release following inhibition of mitochondrial respiration at the level of cytochrome oxidase. Thus, elevated NO production leading to mitochondrial dysfunction, glutamate release, and excitotoxicty may contribute to neuronal death in neurological diseases.
Revue / Journal Title
Journal of neurochemistry ISSN 0022-3042 CODEN JONRA9
Source / Source
1998, vol. 70, no4, pp. 1541-1546 (29 ref.)

INIST-CNRS, Cote INIST : 4037, 35400007527188.0230

My 5 1/2 year old son began taking 4mg Singulair in the p.m. and an inhaler (asmanex) in the a.m. We were still having trouble controlling the asthma and his Sing dose was raised to 5mg. & within 1 week of the increase he began having terrible facial tics and aggravated behavior (defiant, poor listening, easily frustrated and angered) The tics were in the form of opening and closing his mouth, as if you were trying to clear your clogged ears after a plane flight. This caused him much pain in his jaws and facial muscles, so he would tic and then cry as he was in pain. This ramped up his anxiety and it made the ticking worse. He has been off of all asthma medication (cold turkey) for 5 full days. He has episodes where the tics happen for 10 min -1/2 hr, other times during the day it is one here and one there. He does not want to leave the house to do anything, even his favorite activities. Thank god I found this site (and others like it), as I got some answers and some hope. We went to see my cousin this week who is a neurologist and he never heard of the correlation of Singulair and neurologic side effects like these. He said that (hopefully) the medication side effects will cycle through and resolve the ticking and behavioral changes. If not we are probably looking at a Tic Disorder which is in the Tourettes Family.He put my son on a very low dose of Klonopin to mellow out his anxiety and help reduce the tics, but has only been on it for 1 1/2 days and it usually takes a wk or 2 for full absorption and results.I have since sent him and my pediatrician and allergist links to this site and others. I think that I see some improvement in my son, yesterday I thought he did better and my husband thought it was a worse day, I think we have totally lost our perspective and objectivity on this. If anyone out there has a time frame on when they saw significant recovery and positive changes I would love to hear from you. This is a total nightmare and if it is this drug, someone is going to pay. My prayers go out to all who are going thru this.

I have stated many times that I am not an expert. I just post what I find. This has been a mind boggling journey for me. This is way over my head but I struggle to read and understand. Finding answers to why children are suffering from neuro-psychiatric side effects is worth the effort.

I have made the following observations.

1. Some quinoline are known to be able to cross the blood brain barrier.
2. Molecules that ionize are known to be more likely to be able to cross cell membranes. So if montelukast ionizes as a result of change in blood pH to sufficient acid conditions that it ionizes, then it could be possible or maybe like that it does in fact cross the blood brain barrier.
3. We know that there are cysLT1 receptors in the brain.
4. We know that researchers believe that montelukast may bind at the arginine of the cysLT1 receptor.
5. We know that arginine contains four nitrogens. And montelukast contains one.
6. We don't know what happens to those nitrogens.
7. We do know what macrophages create nitric oxide as I posted.
8. We do know that if something cause excessive nitric oxide to build in the brain that there would be damage to the neurons.

Some people may remember when I got stuck at the astrocytes, the cysLT1 receptors and glutamate. I keep looking for research reports that may shed more light on this.

Titre du document / Document title
Nitric oxide causes glutamate release from brain synaptosomes
Auteur(s) / Author(s)
MCNAUGHT K. S. P. (1) ; BROWN G. C. (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Biochemistry, University of Cambridge, Cambridge, ROYAUME-UNI
Résumé / Abstract
We determined the ability of pathological levels of nitric oxide (NO) to cause glutamate release from isolated rat brain nerve terminals using a fluorometric assay. It was found that NO (0.7 and 2 μM) produced (4 and 10 nmol/mg of synaptosomal protein) Ca2+-independent glutamate release from synaptosomes (after 1 min of exposure). Spermine/NO complex (spermine NONOate; a slow NO donor) and potassium cyanide (an inhibitor of cytochrome oxidase) also caused Ca2+-independent glutamate release. Preincubation of synaptosomes with 5 μM 1H- oxadiazole quinoxalin-1-one (an inhibitor of soluble guanylyl cyclase) had no effect on NO-induced Ca2+-independent glutamate release. Ca2+-independent glutamate release produced by NO was greater in a low-oxygen medium. NO, spermine NONOate, and potassium cyanide inhibited synaptosomal respiration with a similar order of potency with respect to their ability to cause glutamate release. Because NO has been shown previously to inhibit reversibly cytochrome oxidase in competition with oxygen, our findings in this study suggest that NO (and cyanide) causes glutamate release following inhibition of mitochondrial respiration at the level of cytochrome oxidase. Thus, elevated NO production leading to mitochondrial dysfunction, glutamate release, and excitotoxicty may contribute to neuronal death in neurological diseases.
Revue / Journal Title
Journal of neurochemistry ISSN 0022-3042 CODEN JONRA9
Source / Source
1998, vol. 70, no4, pp. 1541-1546 (29 ref.)

INIST-CNRS, Cote INIST : 4037, 35400007527188.0230

Hello all! My 9 year old son has been taking Advair inhaler for about 1 1/2 years with 2 puffs a day. One at night and one in the morning. He is too young for him to notice any symptoms and for him to explain them to us and we didn't know about any side effects until reading this forum. He has the sniffles all the time which sound kind of stuffy too and some blotched skin on his forehead. He also might have another symptom regarding his bowels, not being able to control them is what I'm getting at and everyday has accidents. I don't know if that's because of Advair or laziness. I would make an intelligent guess and relate it to the Advair under muscle spasms? Does anyone have this symptom and are just too embarrassed to tell your doc? I am at my wits end with this "symptom". Also I heard very strong reports that cow milk is responsible for asthma. Humans were not designed to drink animal milk at all. The Molecules are way too large for us to digest. Almond milk is best and better for you. Now think about it, we are the only species that drink milk after we are nursed from out mothers. The animals do not go back to drinking after they are weened. I've also heard a study that after grown cows drink cow milk they got very sick or died. Anyone else heard that?

If you question why I don't seem to know everything up to date, this isn't my area of expertise. But, there are thousands of people who probably study related molecules that WONDER WHAT THE F IS GOING ON????

DOES EVERYONE KNOW THIS IS A BRAZILIAN SNAKE VENOM. Just search under Lisinopril and snake venom and watch what comes up. When I took this I went to the herbal store and took herbs for my kidneys and heart, because this med I read can damage them and I did not know what damage was done after 3 months.