The plasmatic levels of coenzyme Q10 and alpha-tocopherol displayed a similar trend-to-depletion in both patient subgroups versus controls. Figure 6(c) reports results of ubiquinol (CoQ10H2, the reduced form of coenzyme Q10) analysis which, together with levels of total CoQ10 (reduced + oxidized forms) and of alpha-tocopherol (both groups of data not shown)—showed similar trend of reduction for EHS as well as MCS subgroups, as compared to CTR group, though lacking statistical significance. Indeed, we found a higher percent coenzyme Q10 oxidation (ratio oxidized-CoQ10/total-CoQ10), significant versus CTR at P < 0.001 in EHS patients, not confirmed for MCS patients, as reported in Figure 6(d).
In detail, the percent levels of the omega-6 FA linoleic (18:2ω6), alpha linolenic (18:3ω6), arachidonic (C20:4ω6), and the omega-3 FA docosahexaenoic (C22:6ω3) (Figures 8(a)–8(d)) were lower than control values in both EHS and MCS cohorts, although the clear-cut statistical significance registered for the MCS group (P < 0.05–0.001 for all 4 parameters) was confirmed in EHS patients only for linoleic acid fraction (P < 0.001) (Figure 8(a)).
The comparative analysis of the fatty acid (FA) profiles in the erythrocyte membranes of the 3 studied groups showed elevated levels of the saturated and monounsaturated fatty acid fraction (SFA) for both environmental-sensitive patients (Figure 7(a)) and correspondingly depleted levels of the polyunsaturated fatty acid fraction (PUFA) (Figure 7(b)), with both parameters statistically significant at P < 0.05 for MCS patients versus controls, whilst the EHS group differed sensibly from MCS in displaying only a mild trend-to-alteration of fatty acid patterns versus control group.
In fact, moving from published data accounting for the altered redox balance in favor of a prooxidative and proinflammatory state in patients with fibromyalgia or chronic fatigue symptoms [7, 22], we identified a profile of 12 specifically altered blood parameters connected with systemic oxidative stress and impaired detoxification, in a representative sample of the Italian population fully or partially complying with MCS diagnosis .
Allele and genotype frequencies of CYPs, UGT, GSTM, GSTT, and GSTP were similar in the Italian MCS patients and in the control populations. The activities of erythrocyte catalase and GST were lower, whereas Gpx was higher than normal. Both reduced and oxidised glutathione were decreased, whereas nitrites/nitrates were increased in the MCS groups. The MCS fatty acid profile was shifted to saturated compartment and IFNgamma, IL-8, IL-10, MCP-1, PDGFbb, and VEGF were increased.
So, it looks like the state of the body has shifted towards pro oxidation, which when further oxidation occurs from chemicals and radiation, becomes overwhelming. That's what it seems like from these studies. I'm sure there has to a be a way to reverse the trend..
Low PUFA: could possibly be remedied by eating avocadoes?.
Low glutathione and low Coq10: Supplements
Linoleic acid: flaxseed oil.
Low Arachidonic acid: eat peanuts.
Omega 6 LA : primrose oil
DHA: Algae - Certain algae are natural sources of DHA and EPA. While most people believe that fish produce their own DHA and EPA, in fact, it’s the algae in their food chain that makes them a rich source of these omega-3s.
I think the fatty acid profile is one of the keys in this study and have long suspected some kind of fatty acid imbalance even before knowing about EHS. This imbalance causes oxidation to be caused more easily and the slightest thing causes excess oxidation. I think people with better balance are more protected and don't get as much oxidation happening when they are around EMFs .
I found consistently that coconut oil which is monosatured caused the problems to get worse.
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