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TOPIC: MCS ag Etiology: A Straight Line

MCS ag Etiology: A Straight Line 8 years 11 months ago #1

TRPA1: Nassini 2011, Deering-Rice 2011, Taylor-Clark 2010, Caceres 2009, Bessac 2008

The Etiology of MCS has been presented formally and documented on the website - here is an informal synopsis.

Much effort has been made to attribute MCS to genetics in detox enzymes - studies in 2007 and 2004 suggested possibly an association. But they were far from conclusive. Studies in 2010 with larger diagnosed MCS groups proved that genetic variants in detox occur no more often in MCS people than in the general population. Detox has become dysfunctional in MCS but not due to genetic cause in detox enzymes.

Such variants may occur in an MCS group but no more often than among others - that is respecting evidence - making decisions - instead of going in a circle.

I've asked persons publishing on this subject why they keep with false conclusions - but have received no constructive acknowledgement - and they may not have corrected those statements.There is so much evidence we should be in close agreement on this disease.

The next circle concerns nitric oxide - super oxide - and peroxynitrite formation (OH N00). Nitric oxide is a normal cellular response. In MCS NO is excessive - and apparently more peroxynitrite formation. In other words, there is oxidative stress - which is major in MCS. But overproduction of nitric oxide is common to many diseases and conditions. It is not what makes MCS unique - and does not account for why MCS develops. It is major and fundamental in the expression of disease but it doesn't explain origin of cause in MCS.

Its not detox enzymes - though they eventually go into dysfunction - and not OH NOO until too late.

The nervous system is the signal caller - peripheral airway transmits to central. MCS people are genetically sensitive - their sensory nerve irritant receptors have always set off more inflammation than the majority of the population. An MCS airway has multiplied nerves - like a gang of revelers trying to grab all the intoxication they can. You want to be sober - but your airway wants to imbibe. Mice with more such receptors inflame and can't stand air pollution.- while their counterparts are saying: What? Me Worry?

MCS nerves multiplied - nerve growth factor and substance P documented through the roof - when the receptors activate so does inflammatory response - the body gets a high reading from the nerves and there is too much release - substances detox has to deal with and drives oxidative stress.

Why keep going in circles - continuing to state this disease is poorly understood - more studies, ideas for drugs, and minimal lifestyle changes? Are we to continue taking a 4000 lb toxic emitting machine with us everywhere - exposure to pollutants documented as driving inflammation of nerves and oxidative stress - and therefore diseases including MCS, Alzheimers, and Parkinsons.

Recent findings are dramatic. Abolishing the response of nerve receptor TRPA1 blocks head pain. With MCS - exposed receptors in the airway transfer misery to the CNS - beginning with TRP through NMDA and involving SP, NGF, cytokine, and NO overproduction. The CNS hurts and registers abnormal - if you want to get morbid and measure.

Decades of exhaust and smoke activate receptors during a subacute phase of predisposition - the airway develops gaps in the epithelium - pollution components can penetrate to the CNS directly with the neurons. The latter point is generic -not genetic! With enough exposure anyone can breakdown and have more penetration to the brain - what makes MCS is reaction of exposed nerves.

It is hopeless with denial of this problem. Researchers suggest the purpose is for developing a treatment - while we continue a sickly environment and no hope for a sound future.

Hundreds - if not thousands of studies - worthless without doing right based on this awareness. We know the cause of MCS.

Statements denying pollution caused disease are not in reality.

Inflammatory chain reactions are turned off if the pollution input is removed. How about 20 MPH bumper cars - fuel cell or electric - no high speed accidents and pollutant emissions.

Rather than stop the nonsense - barbaric studies are performed - laboratory animals are submitted to experiments concerning effects of these poisons while fuels continue to burn for transportation - in principle unwise as smoking in hospitals 30 years ago - and very much as harmful.

This is not a disease of genetic defect such as in detox. That position says life is good - its a shame I have this defect. MCS people are a genetically sensitive subset - a decent environment would have been no problem.There is failure to be honest with these facts - whether consciously intentional or not.

Every day there is horrible air. The only air we know is exhaust and smoke. It is absolute delusion to overlook this reality. Is anyone willing to put aside prestige, career calculations, financial motives, or loyalty to this polluting, high speed lifestyle to be honest about the straight line proof of MCS and the sum total of environmental implications?

Impossibly Good City Design



Bessac B.F. and Jordt S.E. Breathtaking TRP channels: TRPA1 and TRPV1 in airway chemosensation and reflex control. Physiol 23: 360-70 2008

Caceres A. et al. A sensory neuronal ion channel essential for airway inflammation and hypereactivity in asthma. PNAS 106;22: 9099-9104 2009

Deering-Rice C. et al. Electrophilic components of diesel exhaust particles (DEP) activate transient receptor potential ankyrin-1 (TRPA1): a probable mechanism of acute pulmonary toxicity for DEP. Chem Res Tox 24;6:950-9 2011

Nassini R. et al. The 'headache tree' via umbellone and TRPA1 activates the trigeminovascular system. Brain doi:10 1093/brain/awr272 2011

Taylor-Clark T. & Undem B. Ozone activates airway nerves via the selective stimulation of TRPA1 channels. J Physiol 588;3:423-33 2010

Tags: MCS, TRPA1, chemical, etiology, irritant, multiple, receptors, sensitivity, sensory
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