The Latest Study on the effects of masts from the Dept of Psychology at the University of Essex.
Comments on this study from Dr George Carlo
'The following comments relate to the interpretation of the results of the Essex study.
1. Based on what we have learned from our clinical experiences and the symptoms reported by patients in our registry, a key to the integrity of the Essex study is in how a 'sensitive' person was defined at the outset. We believe that the pathology of these sensitivities is cell membrane based, but that the same pathology is present in conditions including multiple chemical sensitivities, alcoholism, drug addiction, and neuro-behavioral syndromes like ADHD and Autism. In addition, there appears to be a familial predisposition component that involves inability to clear metals from the system through methylation and an inability to adapt to oxidative stress.
Thus, the definition of patients selected in the Essex study is a key point. And, in the analyses, it would be important to categorize the patients on the severity scale in terms of these other conditions that have similar underlying pathology. The point is that there is a continuum we are seeing in terms of severity of effects, and the level of hypersensitivity to the various types of EMR also scales along that continuum. Thus, without either controlling for these other conditions statistically or through subject category restriction, it is likely that associations that are present would not be identified.....false negative findings because of imprecision in the measurement of the dependent variables. That is one of the main difficulty with the majority of provocation studies that have been done. Measurement imprecision and bias toward the null.
2. The other key is that depending on the severity of the hypersensitivity...and that in large part is related to the points raised above....different EMR effect windows will have varying effects on the persons being provoked with EMR. Thus, the EMR that is used in the exposure scenario needs to be precisely defined as well. We know, for example, that ELF operates through a field intensity dependent mechanism that exerts direct magnetic effect on tissue (including disruption of gap-junction intercellular communication) and thus the ensuing pathology. But there is a threshold for ELF effects. RF has two different pathology mechanism
components: raw microwaves or RFR act through thermal mechanisms dependent on field intensity -- there is a thermal effects threshold; microwaves that carry information from wireless devices act through a biological mechanism that is triggered as a protective cellular response -- for this response, there is no threshold. Thus, in the Essex study, the provocation exposures would have needed to be defined along these effect windows, otherwise there is a likely bias also toward false negative findings because of the lack of precison in the measurement of the independent variables. For example, from what they define, the question of base station 'on or off' is key. For the effect windows of ELF and raw microwaves, 'on or off' would have an effect if there was adequate field intensity to provoke the mechanistic pathways -- in other words to go above the threshold. However, for the information carrying radio waves, there would have to be talking on the signal or there would be no biological protective pathway triggered. It is the modulation associated with the carried information that we now know triggers the non-thermal effect pathways. So, without talking on the signal, the biological pathway would not be triggered. The result in the study would be a false-negative finding.
3. Overall, the electrohypersensitivity response is dependent then on the severity of the patients cellular pathology -- and that from all sources including the conditions detailed in Number 1 above. The observed response is also dependent on the mechanism that the EMR exposure provocation likely will act through. At this point, we don't believe that a precise enough definition of the conditions in the patients recruited to allow for proper controlling. We don't believe that the exposure provocations were defined well enough in terms of EMR effect windows and the likely pathological pathways triggered by the provocations.
Because of the imprecision in the measurements in the Essex study, any findings showing 'no effect' are likely false negative or the result of the study not being able to pick up the real underlying pathology. Any finding showing an 'effect' is likely an underestimation of the actual effect because the study is biased toward the null or 'no effect' finding.'
Dr. George L. Carlo
Science and Public Policy Institute
1101 Pennsylvania Ave. NW -- 7th Floor
Washington, D.C. 20004