October 22th
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 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
-- By concernedcitizen | Reply | (6) replies | Private Message me
September 16th
2008
9:13 PM
I took reglan in 1990 for the treatment of escophagitis (sorry if spelling is wrong). Had severe life threatening reaction (acute dystonic) and was rushed to hospital. Basically, it started the day after taking it. My face was stuck in a permanent Joker-like smile and it was painful. Thought I was going nuts, I was only 18 at the time, and then took another pill as prescribed. Later, my face stuck in an open mouth gaze position, I could not shut my mouth, it would spring right back open. Then, I lost my speech and spoke like a baby. At that point, my parents realized there was something seriously wrong (they had previously thought it was just me being nervous or something) and called the doctor. I was rushed to the hospital, and on the way I couldn't breathe. My bottom jaw shifted to the right, and my top jaw shifted to the left, and the pain was excruciating. I chipped my front tooth right off. My face was all twisted.
This went away after I was given Benadryl in the ER but I then developed the facial tic associated with Reglan, on the left side of my face. I am 36 years old now and a trial lawyer and singer who is always in the public eye. Luckily, the twitch is slight and only affects my left side, and mostly when I speak because it involves muscle movement. I was prescribed this drug 14 years before it was approved by the FDA. I would tell everyone I know never to take this drug, not even once. Its so dangerous and if I knew of the side effects I would have ever agreed to take it. Its very, very embarrassing to have this twitch. No one ever told me how dangerous this drug was. Hope this post may help someone. Thanks for reading.
-- By vlgiglio | Reply | Private Message me
May 27th
2009
9:40 PM
hey everyone,
Im so glad that I found this forum and that im not the only one feeling like this. I have been on Yasmin now for about 3 years and am coming off it immediately after reading that so many people are having the same side effects. I initially began Yasmin after I had found fibroadenomas in my breast and had to have them removed, and also bad stomach cramps. Taking Yasmin was to regulate my hormones and stop the lumps and cramps. It began really good for me, skin cleared up, no weight gain, and no other side effects. But in the last year it has been a real problem for me and there is nothing else in my lifestyle that would suggests otherwise. I have always had really thick hair and I have lost an incredible amount to the point people are noticing (im so devastated bout this particular side effect as every knew me for my thick straight hair), my heart has irregular palpitations, im badly short of breathe all the time to the point im gasping for air with an open mouth and puffed out just climbing stairs when im not even a smoker, I have a lowered sex drive and really bad lubrication which is a real problem. My attitude has changed and im not my usual easy going self and always looking for an issue to pick at.
I have another month and a half worth but im not going to continue with it. I should have listened to my body earlier or at least known how it has effected so many other people.
I understand that it works really well for some people but it seems to not work for just as more people, which makes me wonder why it is so readily pushed onto patients by doctors when there should be clear warnings. The attractive point for me when my doctor suggested Yasmin was that it had been tested to have NO side effects......yeh ok!
-- By munkyfunk | Reply | (1) replies | Private Message me