Scientists and physicians are on their way to identifying the means to screen electrohypersensitive (EHS) patients via blood panels, as this 2014 study explains. In this study, preliminary results identified genetic markers predisposing individuals to development of EHS. (CEP Director)
Growing numbers of “electromagnetic hypersensitive” (EHS) people worldwide self-report severely disabling, multiorgan, non-specific symptoms when exposed to low-dose electromagnetic radiations, often associated with symptoms of multiple chemical sensitivity (MCS) and/or other environmental “sensitivity-related illnesses” (SRI). This cluster of chronic inflammatory disorders still lacks validated pathogenetic mechanism, diagnostic biomarkers, and management guidelines. We hypothesized that SRI, not being merely psychogenic, may share organic determinants of impaired detoxification of common physic-chemical stressors. Based on our previous MCS studies, we tested a panel of 12 metabolic blood redox-related parameters and of selected drug-metabolizing-enzyme gene polymorphisms, on 153 EHS, 147 MCS, and 132 control Italians, confirming MCS altered –0.0001) glutathione-(GSH), GSH-peroxidase/S-transferase, and catalase erythrocyte activities. We first described comparable—though milder—metabolic pro-oxidant/proinflammatory alterations in EHS with distinctively increased plasma coenzyme-Q10 oxidation ratio. Severe depletion of erythrocyte membrane polyunsaturated fatty acids with increased ω6/ω3 ratio was confirmed in MCS, but not in EHS. We also identified significantly altered distribution-versus-control of the CYP2C19*1/*2 SNP variants in EHS, and a 9.7-fold increased risk (OR: 95% C.–74.5) of developing EHS for the haplotype (null)GSTT1 + (null)GSTM1 variants. Altogether, results on MCS and EHS strengthen our proposal to adopt this blood metabolic/genetic biomarkers’ panel as suitable diagnostic tool for SRI.
… in the GST study we now compared EHS and healthy controls. Differently from our previous results on MCS, we here identified a mutated (null) allele combination of GSTT1 and GSTM1 variants able to predict risk of developing EHS by a 9.7 fold versus CTR (Table 1).
Taken together, our genetic results obtained on a number of cases due to be enlarged in the studies to come, although being far to be conclusive on such a controversial matter, can at least contribute additional indications to the complex mosaic of genetic risk factors in environmental hypersensitivities, still waiting to be correlated with individual metabolic phenotypes.
The outcomes of this work confirmed, in the whole, our previous results on MCS and provided additional evidences for the validity of the selected panel of metabolic blood parameters also in the self-reported EHS condition. Further developments must necessarily include a more objective and standardized classification of individual electromagnetic sensitivity scores, to conclusively assess the proposed parameters as a distinctive and specific panel of disease biomarkers for EHS. Our findings will hopefully contribute, in combination with the so-far putative genetic-risk factors, a better molecular definition of environmental-borne sensitivity-related illnesses and a tool to discriminate single SRI comorbidities, based on sufficiently proven molecular evidences able to gain clinical consensus.