My 5 1/2 year old son began taking 4mg Singulair in the p.m. and ...

The fact that increased dosage caused neurological damage made me think of my post from June. Many studies were done about how montelukast metabolizes in the body. If the dosage was increased to a level of excess that was not immediately controlled by the body's liver enzymes to break down the montelukast molecules, then maybe my theory has some validity. If montelukast penetrated the blood-brain barrier during the period of excessive dosage, then montelukast was maybe the cause of your child's neurological symptoms.

This may be something to discuss with your cousin, the neurologist.

2008
4:57 PM
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 excitotoxicty 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

What do I think that I know that I am not saying?

a. It would seem that the original researchers were looking for a medication to control asthmatic episodes as a result of fungus, aspergillus and other smaller varieties.
b. The body's own defense mechanism against these types of organism is the chemical nitric oxide which is produced by macrophages - the mast cell.
c. The time period of the original research on montelukast coincided with the nobel prize for work regarding the function of nitric oxide in the body. Often researchers are interested in the same areas at the same time--and are in competition with other groups for discoveries.
d. I suspect that montelukast is a chemical substitute for the natural production of nitric oxide in the body. And, that certain individuals lack adequate function of this mechanism in their body thus they suffer from defective immune systems.
e. Singulair is a dangerous drug for individuals who are not in the correct category. So, those individuals who suffer side effects are suffering for a good reason. That reason is that they are not compatible with the pharmaceutical (for lack of a better word) MODEL for this drug.

Please visit us at www.parentsforsafety.org to view posts about recovery from Singulair and other information.
Jenna

Hi
My son had that same tick, I sent you a private email about it so please check.
Thanks

unbelievable- to fix your child's anxiety caused by one drug- they put him on another drug! why not just let him detox? the last thing he needs is more drugs. sounds like some doctor had to make a mortgage payment. niacin will reduce anxiety and try natural things like diet to help with his asthma

I would advise all parents to pay very close attention to this drug and it affects on your children. I read the side affects but thought they would not apply to our son. A friend of mine told me that she heard that it caused death in boys. Well, that sounded weird. I researched it and found this information. We decided to stop giving it to our 2 year old son. He'd been irritable and very short tempered. he is aggravated and aggressive. All of these symptoms appeared after the use of Singulair. He says he sees things when there is nothing there. He used Singulair from November 23 until Jan 3 2009. I am appalled that the asthma specialist prescribed this medication as a last attempt to resolve his asthma before going to a pulmanologist.