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A long standing problem for people with environmental illnesses, such as MCS and EHS, has been the lack of recognized biomarkers for the health conditions. A research team in Paris, France, managed by Dr. Dominique Belpomme, has published a paper that appears to fill that need. The full title is -
This paper begins with a general survey of our society's past problems in accepting MCS and EHS as physical health conditions, going back to Dr. Randolph's description in the 1960's. It mentions that MCS was formally recognized in an international concensus in 1999 to be the following -
This research group has, since 2009, clinically investigated more than 1200 EHS and/or MCS self reporting cases to develop a better understanding of the health conditions. They found that, of these patients, some 71.6% were diagnosed with EHS, 7.2% with MCS, and 21.2% with both EHS and MCS.
They regard changes in the following body chemicals as biomarkers for MCS and EHS -
Increased High Sensitivity C Reactive Protein was common, suggesting some type of systemic inflamation. None was found, but this marker is also considered a biomarker for Alzheimer's disease.
There were common deficiencies for vitamins D2, and D3.
A common and important finding was that histamine was increased im many patients. Histamine is a both a neurotransmitter and an inflamatory mediator for many inflammatory processes.
IgE levels were commonly increased which suggests a body-wide inflammation.
Levels of Protein S100B were commonly increased in the patients. This is a biomarker of hypoperfusion that is associated with brain dysfunction or damage. It is also suggestive of Alzheimer's disease.
Nitrotyrosin, a marker of both peroxynitrite (ONOO) production and opening of the blood-brain barrier (BBB), was increased.
Circulating autoantibodies against O-myelin were detected, which may be associated with autoimmune response.
The Hsp27 and/or Hsp70 heat shock proteins were increased; more frequently in EHS patients than MCS patients.
Chronic insomnia and fatigue are common in patients with MCS and EHS. Using the 6-hydroxymelatonin sulfate (6-OHMS)/creatinin ratio, it was found and that melatonin was significantly decreased in all patients. But instead of the decrease coming from the pineal gland (which makes melatonin), it appeared that the decrease was caused by melatonin being used as a free radical scavanger by the body.
The brain blood flow in the temporal lobes was actually measured with pulsed cerebral ultrasound computed tomosphygmography. Both EHS and MCS disorders were associated with hypoperfusion in the capsulothalamic area. That suggests that the inflammatory processes involve the limbic system and the thalamus areas of the brain.
Both disorders appear to involve inflammation-related hyper-histaminemia, oxidative stress, autoimmune response, capsulothalamic hypoperfusion and Blood Brain Barrier opening, and a deficit in melatonin metabolic availability; suggesting a risk of chronic neurodegenerative disease. Finally, since EHS and MCS usually occur together, this suggests a basic common pathological mechanism for both EHS and MCS.
EHS and MCS can now be objectively characterized and routinely diagnosed by simple commercially available tests.
The article is some 20 pages long and available at -
Dr. Belpomme's web site to support EHS and MCS -
Dr. Belpomme's professional web site -
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