Multiple chemical sensitivity: Genotypic characterization, nutritional status and quality of life in 52 patients

Food Implications in Central Sensitization Syndromes

“…In addition, environmental factors and genetic components are involved in the development of CSS. In fact, several single nucleotide polymorphisms related to the presence of FM, CFS and MCS have been described [ 2 , 6 ]. Indeed, it has been hypothesized that specific genetic profiles of impairment in certain essential enzymes are involved in the optimal corporal endobiotic/xenobiotic detoxification (phase I and II), DNA methylation/repair pathways and antioxidant defense/oxidative stress, such as CYP450, GST, NAT2, MTHFR, SOD2, PON1, PON2, NOS2 and NOS3 genes [ 2 ].…”

“…Indeed, it has been hypothesized that specific genetic profiles of impairment in certain essential enzymes are involved in the optimal corporal endobiotic/xenobiotic detoxification (phase I and II), DNA methylation/repair pathways and antioxidant defense/oxidative stress, such as CYP450, GST, NAT2, MTHFR, SOD2, PON1, PON2, NOS2 and NOS3 genes [ 2 ]. A case in point, statistically significant differences in the frequencies of MTHFR rs1801133 were observed in a descriptive study composed of 52 MCS patients and 52 healthy volunteers by Loria-Kohen et al [ 6 ]. Similarly, this single nucleotide polymorphism was related to MCS in another study by Micarelli et al in MCS patients that also found an association with some functional polymorphisms in genes affecting enzyme function, such as MTHFR rs1801131, SOD2 rs4880, NOS3 rs1799983, PON1 rs705379 and rs 662 [ 2 ].…”

“…The use of dietary components with potential functionality on inflammation (i.e., flavonoids, vitamin D or n-3 fatty acids) and oxidative stress (i.e., magnesium, selenium, zinc, vitamin A, C and E or coenzyme CoQ10) seem promising in the treatment of these patients due to the alterations in oxidative stress and neuroinflammation that they may suffer. However, the scientific literature is contradictory regarding dietary and nutritional management [ 6 , 8 ].…”

The SNP rs2298383 Reduces ADORA2A Gene Transcription and Positively Associates with Cytokine Production by Peripheral Blood Mononuclear Cells in Patients with Multiple Chemical Sensitivity

“…Indeed, dramatically increased levels of reactive oxygen and nitrogen species (ROS, RNS), as well as pro-inflammatory cytokines and the presence of autoimmune antibodies, have been reported in MCS patients compared with healthy subjects [9][10][11][12][13][14]. Moreover, a link has been suggested between MCS and inherited or acquired defects in genes coding for enzymes involved in xenobiotic metabolism phase I and II, antioxidant defense, lipid metabolism and one-carbon pathway [11,12,[15][16][17][18][19][20][21]. The presence of polymorphic variants of xenobiotic-metabolizing enzymes, other than raising the risk of serious adverse reactions to drug treatment, can also increase the individual sensitivity to the environmental toxic burden, determining the development of chronic systemic oxidative stress and inflammation.…”

A case report of idiopathic environmental intolerance: A controversial and current issue

“…Others have instead shown peculiar genetic polymorphisms that can explain the symptomatology. In this regard, although in literature it is reported that 26 genes are implicated in the pathogenesis of MCS, but only a few of these are important . This group includes mutations of the catalase coding gene (CAT C262T homozygosity polymorphism) and of the gene encoding glutathione transferase (polymorphism with a null genotype of the GSTT1 gene and heterozygosity polymorphism of the GSTP1 A313G gene) that seem to increase cellular oxidative stress after exposure to certain xenobiotics and to facilitate the onset of bronchial hyperactivity and asthmatic‐like symptoms in patients with MCS .…”