Dr. Weeks’ Comment: Whatever the initial insult or injury, the damage is spread via inflammatory pathways and mechanisms. Now we see a role for safe andeffective anti-inflammatory agents in the treatment not only of schizophrania and depression ( see slides on depression and schizophrenia) but also of multiple chemical sensitivity (MCA). The best anti-inflammatory agent is…. clean pure water… (no fluoride no chloride, no heavy metals no pesticides etc!) but second best is SOUL !
An elevated pro-inflammatory cytokine profile in multiple chemical sensitivity.
Psychoneuroendocrinology. 2014 Feb;40:140-50. doi: 10.1016/j.psyneuen.2013.11.012. Epub 2013 Nov 24.
Author information ”¨”¨”¨Abstract”¨”¨
Multiple chemical sensitivity (MCS) is a medically unexplained condition characterized by reports of recurrent unspecific symptoms attributed to exposure to low levels of common volatile chemicals. The etiology of MCS is poorly understood, but dysregulation of the immune system has been proposed as part of the pathophysiology.
To compare plasma levels of cytokines in Danish MCS individuals with a healthy, sex- and age-matched control group.
Blood samples were obtained from 150 un-exposed MCS individuals and from 148 age- and sex-matched healthy controls. Plasma concentrations of 14 cytokines, chemokines and growth and allergen-specific IgE were measured. All participants completed a questionnaire including questions on MCS, psychological distress, morbidities and medication use at the time of the study.
Plasma levels of interleukin-1ÃŽ², -2, -4, and -6 were significantly (P<0.001) increased in the MCS group compared with controls, tumor necrosis factor-ÃŽ± was borderline significantly (P=0.05) increased and interleukin-13 was significantly decreased (P<0.001).
MCS individuals displayed a distinct systemic immune mediator profile with increased levels of
pro-inflammatory cytokines and interleukin-2 and inverse regulation of Th2 associated cytokines interleukin-4 and interleukin-13 suggestive of low-grade systemic inflammation, along with a deviating Th2-associated cytokine response not involving IgE-mediated mechanisms.